Preclinical studies have indicated that synergistic effects can be achieved by combining CDK9i with agents targeting BCL‐2, MDM2, PARP, BTK, EGFR, BET or BRD4, glucocorticoid receptor, and chemotherapeutic drugs such as temozolomide and 5‐fluorouracil.[37] Our drug synergy studies demonstrated that co‐targeting of CDK9 and KRAS/MAPK signaling pathway eliminated ERK‐MYC activation and prevented feedback activation mediated by receptor tyrosine kinases, leading to enhanced efficacy of KRAS‐mutant cancers and overcoming KRASi resistance. The gene discussed is BCL2; the disease is cancer.