Increased SYK phosphorylation in mutant CBL‐expressing cells, which are characterized by hyperactivated wt FLT3, may be reflective of the transactivation and cooperativity between highly activated SYK and constitutively activated mutant FLT3 observed in AML patients.21 The increases in levels/activity of FLT3 in mutant CBL‐expressing cells may be due to failure of mutated CBL to function properly as an E3 ubiquitin ligase9, 10 and may also explain the higher susceptibility of these cells to FLT3 inhibitor treatment. The gene discussed is CBL; the disease is acute myeloid leukemia.