In human colorectal cancer (CRC), series of gene mutations are involved in the tumorigenesis, and the accumulation of genetic and epigenetic alterations are involved in the tumorigenesis.1,2 The tumor suppressor APC functions as a “gatekeeper” and its gene mutations occur at the initiation stage of the colorectal tumorigenesis, and KRAS mutations occur at the early adenoma stage and play roles in the progression of the tumorigenesis.2 The APC and KRAS mutations frequently occurs simultaneously; however, interaction of these two gene mutations in the tumorigenesis is poorly understood. Here, KRAS is linked to adenoma.