Subsequent studies showed that the majority of BCR‐ABL1‐like ALL patients harbor kinase‐activating abnormalities, including ABL‐class fusions, CRLF2 rearrangements, JAK2 fusions, other mutations activating the JAK‐STAT pathway, and mutations of the RAS pathway.3, 4, 5, 6. This evidence concerns the gene SOAT1 and acute lymphoblastic leukemia.