Our findings demonstrate that (1) AZD1775 induces cell death through apoptosis; (2) AZD1775-mediated inhibition of WEE1 alters the anti-apoptotic dependency in DLBCL; (3) combination of AZD1775 with cell-specific anti-apoptotic inhibitors (such as venetoclax) leads to enhanced potency; (4) both DNA damage and G2/M arrest induced by WEE1 inhibition independently enhances dependency on anti-apoptotic proteins. The gene discussed is WEE1; the disease is diffuse large B-cell lymphoma.