P190 BCR-ABL1 can mediate the tyrosine phosphorylation of STAT members, and JAK1 and JAK2 have been found to be constitutively activated by mutations in the kinase and pseudokinase domains, which explains the sensitivity of Ph+ leukaemia cells to JAK2 inhibitors [251, 252]. The gene discussed is SOAT1; the disease is leukemia.