In 1990, some researchers proposed that occurrence of CRC begins with adenomatous polyposiscoli inactivation mutation followed by activation mutation of oncogene Kirsten rat sarcoma (KRAS) and sequential mutation of SMAD family member four, tumor protein p53 (TP53), and phosphoinositide 3‐kinase catalytic subunit‐α. Here, KRAS is linked to colorectal carcinoma.