In RTK‐targeted therapies, such as imatinib targeting mutant KIT in GIST, acquired resistance frequently follows a short‐lived treatment response.28 This predicament urges a fundamental elucidation of the interdependent KIT‐eliciting downstream and collateral pathways essential for sustaining the resistance and survival of tumour cells to develop novel therapeutic strategies.7 In GIST cells harbouring refractory mutations, BRD4 knockout indeed inhibited the activity of the PI3K/AKT/mTOR axis and notably increased the susceptibility to imatinib. This evidence concerns the gene AKT1 and neoplasm.