In HCT116 colon cancer cells that had been genetically manipulated to delete their single allele of K-RAS D13 or in deleted cells engineered to express various forms of H-RAS V12 we found that transformed but non-tumorigenic K-RAS D13 deleted cells were less sensitive to the drug combination whereas H-RAS V12 transfected cells which have hyper-activated both the PI3K and ERK1/2 pathways were more sensitive to the drugs (Figure 1C). This evidence concerns the gene HRAS and malignant colon neoplasm.