Thus, the limited clinical efficacy of WEE1 inhibitor monotherapy suggests an urgent need for novel combination strategies, such as chemotherapy plus AZD1775 for TP53-mutant ovarian cancer [180], chemotherapy followed by AZD1775 maintenance for TP53/KRAS-mutant CRC [181], AZD1775 plus an inhibitor of histone deacetylase (HDAC) or bromodomain-containing protein 4 (BRD4) for acute leukemia [182], or dual blockade of WEE1/AXL receptor tyrosine kinase (AXL) or WEE1/mTOR for SCLC [177]. The gene discussed is WEE1; the disease is acute leukemia.