In imatinib‐resistant GIST cells, stable silencing of endogenous BRD4 decreased cell growth and migration and enabled resensitization to imatinib, concomitant with significant suppression of the activity and/or expression of kinases in the PTEN/PI3K/AKT/mTOR signalling cascade. The gene discussed is BRD4; the disease is gastrointestinal stromal tumor.