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Despite improved survival, targeting drug\u2010resistant leukaemia stem cells (LSCs) remains a challenge for curative CML therapy. Aberrant lipid metabolism can have a large impact on membrane dynamics, cell survival and therapeutic responses in cancer. While ceramide and sphingolipid levels were previously correlated with TKI response in CML, the role of lipid metabolism in TKI resistance is not well understood. We have identified downregulation of a critical regulator of lipid metabolism, G0\/G1 switch gene 2 (G0S2), in multiple scenarios of TKI resistance, including (1) BCR::ABL1 kinase\u2010independent TKI resistance, (2) progression of CML from the chronic to the blast phase of the disease, and (3) in CML versus normal myeloid progenitors. Accordingly, CML patients with low <jats:italic>G0S2<\/jats:italic> expression levels had a worse overall survival. G0S2 downregulation in CML was not a result of promoter hypermethylation or BCR::ABL1 kinase activity, but was rather due to transcriptional repression by MYC. Using CML cell lines, patient samples and G0s2 knockout (G0s2<jats:sup>\u2212\/\u2212<\/jats:sup>) mice, we demonstrate a tumour suppressor role for G0S2 in CML and TKI resistance. Our data suggest that reduced G0S2 protein expression in CML disrupts glycerophospholipid metabolism, correlating with a block of differentiation that renders CML cells resistant to therapy. Altogether, our data unravel a new role for G0S2 in regulating myeloid differentiation and TKI response in CML, and suggest that restoring G0S2 may have clinical utility.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ctm2.1146","type":"journal-article","created":{"date-parts":[[2022,12,20]],"date-time":"2022-12-20T04:22:31Z","timestamp":1671510151000},"source":"Crossref","is-referenced-by-count":17,"title":["Loss of G0\/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolism"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7980-6685","authenticated-orcid":false,"given":"Mayra A.","family":"Gonzalez","sequence":"first","affiliation":[{"name":"Department of Molecular and Translational Medicine Center of Emphasis in Cancer Texas Tech University Health Sciences Center El Paso  El Paso Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9039-5322","authenticated-orcid":false,"given":"Idaly M.","family":"Olivas","sequence":"additional","affiliation":[{"name":"Department of Molecular and Translational Medicine Center of Emphasis in Cancer Texas Tech University Health Sciences Center El Paso  El Paso Texas USA"},{"name":"L. 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