They found that knockdown of the anti-apoptotic BH3 family gene BCL-XL was synergistic with MEK inhibition and targeting BCL-XL with ABT-263 (navitoclax) combined with a MEK inhibitor resulted in dramatic apoptosis in vitro and remarkable in vivo tumor responses in KRASm xenografts [36]. The gene discussed is BCL2L1; the disease is neoplasm.