Instead, BCR-ABL1-driven activation of the JAK/STAT pathway through the phosphorylation of JAK2 has similar effects on both chronic myeloid leukemia (CML) and ALL, whereby pJAK2 and pSTAT5 cooperate to maintain elevated levels of MYC by protecting it from ubiquitin-dependent degradation [60,61]. This evidence concerns the gene SOAT1 and chronic myelogenous leukemia, BCR-ABL1 positive.