Clinical studies with midostaurin have shown that its effects as a single agent are at best partial and transient, and for patients to achieve maximum clinical benefit midostaurin must be administered in combination with other anti‐cancer drugs.14, 38 Highly activated SYK has been observed to be enriched in FLT3‐ITD‐positive patient AML, and its cooperation with oncogenic FLT3 leads to activation of MYC transcriptional programmes.21 Consistent with this, in the present study we observed higher SYK activity in mutant CBL‐expressing cells relative to control cells. This evidence concerns the gene MYC and cancer.