The final product of steroid biosynthesis is cholesterol and oncogene-transformed cancer cells (including KRAS) require elevated levels of cholesterol to support their rapid growth.34,35 Targeting the C4-demethylating genes in the steroid biosynthesis pathway has been shown to sensitise previously resistant cancer cells to the EGFR inhibitors, erlotinib and cetuximab.35,36 Our RNAseq results provide further evidence that oncogenic KRAS CRC cells have an increased dependency on cholesterol biosynthesis. The gene discussed is KRAS; the disease is colorectal carcinoma.