Here, we have considered the possibility that a similar strategy to target SYK in FLT3-mutant patients with AML might also be beneficial, since SYK is required for optimum transformation by FLT3-ITD.6 Interestingly, like FLT3, SYK is known to be a target of the E3 ligase c-CBL, and recent studies show that both FLT3 and SYK are regulated by ubiquitination and deubiquitination, which modulate both protein turnover and function.15–18 However, the DUBs that regulate SYK stability are unknown. The gene discussed is SYK; the disease is acute myeloid leukemia.