The mutated KRAS holds the GTP-bound active state & overcomes the GTPase activity (GTP to GDP hydrolysis), which further continuously promotes cellular proliferation and metastasis in various cancers such as pancreatic ductal adenocarcinoma (PDAC), colorectal adenocarcinoma (CRC), and non-small cell lung cancer (NSCLC) [6, 7]. This evidence concerns the gene KRAS and colorectal adenocarcinoma.