Then, using a DGKα specific inhibitor, CU-3, we also demonstrated synergy with trametinib in MCF10A cells, but in this case, drug dose combinations affected the SCRIBRNAi/H-RASG12V cells similarly to normal cells, suggesting that CU-3 would not be clinically useful in specifically targeting Ras-driven cancer cells. This evidence concerns the gene DGKA and cancer.