In KRAS-mutated NSCLC tumors, Nangia et al. described that concurrent blockade of MEK and MCL-1 synergistically increased cytotoxicity in vitro and in vivo [17]; and in EGFR-mutated tumors, Hata et al. revealed that EGFR inhibitor-resistant cells responded to dual inhibition of BCL-xL and BCL-2 in patient-derived tumor cells [16]. The gene discussed is BCL2L1; the disease is neoplasm.