T‐LAK cell‐originated protein kinase/PDZ‐binding kinase (TOPK/PBK) has been identified as a drug target due to its low expression in most normal tissues and high expression in various tumor types,11, 12 where high TOPK levels correlate with poor patient prognosis.12, 13, 14, 15, 16 Elevated TOPK expression is driven by MYC and E2F1 in high‐grade lymphomas17 and in FLT3‐mutated AML,18 but the mechanism of upregulation in other contexts is not well understood. The gene discussed is FLT3; the disease is acute myeloid leukemia.