Although overexpressed BRD4 has emerged as a potential therapeutic target in various cancer types, knowledge about the biology of BRD4 inhibition in GIST cell and xenograft models is scant.19 One such mechanism hypothesized to be involved in imatinib resistance in GIST is the activation of PI3K/AKT signalling.39 Indeed, there was an increase in the expression of BRD4 in imatinib‐resistant GIST cells in vitro as well as in the imatinib‐resistant tumour specimens of GIST patients. The gene discussed is AKT1; the disease is cancer.