Cholesterol is associated with an increased risk of CRC51 and targeting its synthesis has been shown to sensitise previously resistant cancer cells to the EGFR inhibitors, erlotinib and cetuximab.35,36 Our RNAseq results provide further confirmation that oncogenic KRAS cells have an increased dependency on cholesterol biosynthesis and targeting this pathway could thus be a therapeutic strategy in KRAS mutant CRC patients. This evidence concerns the gene KRAS and colorectal carcinoma.