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In 1930 Streeter stated \u201c apodictically\u201d that no evidence has been found that intra\u2010uterine amputation is due to amniotic bands or adhesions \u2026\u201d and that his 16 cases provided (histological) evidence for a \u201cgerminal origin.\u201d He concluded that an amniotic cord was \u201cnot an adhesion or inflammatory product but \u2026 an anomalous developmental structure and present from the outset.\u201d In survivors the \u201ctraces\u201d of damaged limb\u2010buds \u201creveal the scars of poor germ\u2010plasm.\u201d In 1958, Willis, in dismissing the amniotic origin of the ADAM defects (or \u201cStreeter\u201d or \u201cSimonart\u201d bands) quoted Keith [1940] to the effect that \u201c(a)mniotic adhesions \u2026 are always produced by \u2026 the fetus \u2013 as a result of dysplasia in foetal tissues. They are the result, not the cause, of foetal malformations.\u201d Streeter [1930] mentions a potential familial case (56\u2010year\u2010old man and his mother), not controlled by photographs or other records and concluded \u201cthat the (ADAM) deformity is not easily transmissible,\u201d but \u201cdue to the constitution of the germ\u2010plasm.\u201d Torpin [1968] concluded, as apodictically as Streeter and Willis, that \u201c\u2026 proof of amnion rupture without damage to the chorionic sac is no longer \u201cin question.\u201d Considering Torpin's decades\u2010long study of the ADAM phenomenon and review of 494 references (missing many) it is surprising that he does not discuss the relationship between the apparent ADAM defects and other, internal anomalies that maybe present in an affected fetus or infant not evidently caused by the <jats:italic>a<\/jats:italic>mniotic <jats:italic>d<\/jats:italic>isruptions, <jats:italic>a<\/jats:italic>dhesions or <jats:italic>m<\/jats:italic>utilations, unless his mind was made up. Our review of these internal and other presumed primary malformations in ADAM is ongoing. However, on a preliminary basis, it seems likely to us that: (1) there is an increased prevalence of such primary anomalies in the ADAM condition confirming the view and experience of others, for example Czeizel et al. [1993]; (2) these malformations (e.g., heterotaxy) may arise as early as gastrulation; (3) that, given the ADAM phenomenon is exclusively ascertained as the ADAM phenotype in fetuses and infants, that is, that its cause and ascertainment are completely congruent, then the apparent amniotic defect must also be regarded as a malformation; (4) that in such a case the ADAM phenomenon with associated primary malformation(s) is a form of <jats:italic>syndromal pleiotropy<\/jats:italic> due to one cause yet to be elucidated. To that end we recommend archiving DNA from all affected fetuses coming to autopsy and their parents and placentas and surgical tissues of all viable affected infants for ultimate exome or genome sequencing perhaps with special attention to the <jats:italic>syncytin<\/jats:italic> genes. \u00a9 2015 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ajmg.a.36937","type":"journal-article","created":{"date-parts":[[2015,1,21]],"date-time":"2015-01-21T14:48:46Z","timestamp":1421851726000},"page":"478-503","source":"Crossref","is-referenced-by-count":13,"title":["ADAM \u201csequence\u201d part II: Hypothesis and speculation"],"prefix":"10.1002","volume":"167","author":[{"given":"John M.","family":"Opitz","sequence":"first","affiliation":[{"name":"Department of Pediatrics (Division of Medical Genetics) University of Utah, School of Medicine Salt Lake City Utah"},{"name":"Department of Pathology University of Utah, School of Medicine Salt Lake City Utah"},{"name":"Department of Human Genetics University of Utah, School of Medicine Salt Lake City Utah"},{"name":"Department of Obstetrics and Gynecology University of Utah, School of Medicine Salt Lake City Utah"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis R.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Utah, School of Medicine Salt Lake City Utah"},{"name":"Department of Pathology (Pediatrics) Primary Children's Hospital Salt Lake City Utah"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Enid F.","family":"Gilbert\u2010Barness","sequence":"additional","affiliation":[{"name":"Department of Pathology Tampa General Hospital Tampa Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,1,21]]},"reference":[{"key":"e_1_2_18_2_1","doi-asserted-by":"publisher","DOI":"10.1053\/plac.2002.0934"},{"key":"e_1_2_18_3_1","volume-title":"Manual of antenatal pathology and hygiene: The embryo","author":"Ballantyne JW","year":"1904"},{"key":"e_1_2_18_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/ajmg.1320440304"},{"key":"e_1_2_18_5_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pbio.0060063"},{"key":"e_1_2_18_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/mrd.10073"},{"key":"e_1_2_18_7_1","volume-title":"Gaining ground","author":"Clack J.A","year":"2002"},{"key":"e_1_2_18_8_1","unstructured":"CohrsP.1939. 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