Importantly, PROTACs‐induced BRD9 degradation promotes an antiproliferative phenotype in a pro‐monocytic human myeloid leukemia cell line (U937) better than the well‐known BRD9 degrader dBRD9, reinforcing the valid potential of this pharmaceutical approach as an anticancer therapeutic strategy for the treatment of BRD9‐dependent tumors. This evidence concerns the gene BRD9 and myeloid leukemia.