Furthermore, the venetoclax-S63845 combination potentiated melanoma cell killing caused by the BRAFV600E inhibitor darafenib in BRAF-mutant melanoma cells (Supplementary Fig. S16), suggesting that co-inhibition of BCL2 and MCL1 as a strategy to enhance the induction of apoptosis has broad utility as a means to potentiate the activity of targeted therapies in disseminated human melanomas. The gene discussed is MCL1; the disease is melanoma.