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Whatever their molecular mechanism, hereditary AIDs are caused by mutations in regulatory molecules or sensors proteins leading to dysregulated production of proinflammatory cytokines or cytokine\u2010inducing transcription factors, fever, elevation of acute phase reactants, and a portfolio of manifold inflammatory signs which might occur in a stereotyped manner, mostly with overactivity or misactivation of different inflammasomes. Symptoms might overlap in the pediatric patient, obscuring the final diagnosis of AIDs and delaying the most appropriate treatment. Actually, the fast\u2010paced evolution of scientific knowledge has led to recognize or reclassify an overgrowing number of multifactorial diseases, which share the basic pathogenetic mechanisms with AIDs. The wide framework of classic hereditary periodic fevers, AIDs with prominent skin involvement, disorders of the ubiquitin\u2010proteasome system, defects of actin cytoskeleton dynamics, and also idiopathic nonhereditary febrile syndromes occurring in children is herein presented. Interleukin\u20101 dependence of these diseases or involvement of other predominating molecules is also discussed.<\/jats:p>","DOI":"10.1111\/jebm.12406","type":"journal-article","created":{"date-parts":[[2020,7,6]],"date-time":"2020-07-06T08:12:14Z","timestamp":1594023134000},"page":"227-245","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Phenotype variability of autoinflammatory disorders in the pediatric patient: A pictorial overview"],"prefix":"10.1111","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7032-7779","authenticated-orcid":false,"given":"Donato","family":"Rigante","sequence":"first","affiliation":[{"name":"Department of Life Sciences and Public Health Fondazione Policlinico Universitario A. 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