In venetoclax/HMA-refractory or TP53-mutant AML with replication-stress signatures, prioritize short-pulse ATR (e.g., ceralasertib) or WEE1 (e.g., adavosertib) combinations with marrow-sparing venetoclax windows, guided by γH2AX/CHK1-P pharmacodynamics and MRD kinetics (Bataller et al., 2024). The gene discussed is CHEK1; the disease is acute myeloid leukemia.