It has been reported that the mechanism of BRD4 inhibitor resistance in AML was mainly associated with WNT/β‐catenin–mediated c‐MYC reactivation after suppression, so targeting the WNT/β‐catenin–c‐MYC axis possibly could help overcome BRD4 inhibitor resistance [14]. This evidence concerns the gene MYC and acute myeloid leukemia.