However, incorporating additional biomarkers—such as γH2AX (for DSBs), p-Chk1 (for DDR checkpoint activation) and RAD51 foci assays (for HR repair functionality)—could further refine the representation of drug synergy, saturation and timing effects and cancer cell sensitivity to PARP and ATR inhibitors, improving model predictivity for different dosing strategies in specific tumour types. The gene discussed is CHEK1; the disease is neoplasm.