[147] used CRC patient cohort analyses, homologous cell lines, and transgenic mice to discover that APC/KRAS mutant CRC induces de novo cholesterol synthesis, accompanied by an increase in geranylgeranyl pyrophosphate (GGPP), a metabolite required for KRAS activation, which promotes the development of APC/KRAS mutant CRC through activation of the KRAS/MEK/ERK signaling pathway. The gene discussed is APC; the disease is colorectal carcinoma.