Other JAK-STAT signaling activating mutations are present in approximately 10% of BCR/ABL1-like ALL cases and include JAK2 fusions (translocations or interstitial deletions) that retain the tyrosine kinase domain, EPOR truncating rearrangements (e.g., with IGH, IGK, and LAIR1), IL7R insertion/deletions in the transmembrane domain, and deletions or mutations of SH2B3 (a negative regulator of JAK-STAT signaling, the mutation of which augments JAK-STAT signaling). This evidence concerns the gene SOAT1 and acute lymphoblastic leukemia.