Diverse genetic alterations dysregulating kinase and receptor signaling are the hallmark of the BCR::ABL1-like ALL and can be divided into several classes: (1) alterations activating JAK-STAT pathway signaling (including rearrangements of cytokine receptor-like factor 2 (CRLF2) gene, Janus kinase 2 (JAK2) gene and erythropoietin receptor (EPOR) gene); (2) rearrangements of ABL-class genes (ABL1, ABL2, PDGFRα, PDGFRβ, CSF1R); (3) Ras pathway mutations (KRAS, NRAS, NF1, PTPN11) and other uncommon rearrangements [6, 7, 12]. The gene discussed is SOAT1; the disease is acute lymphoblastic leukemia.