(Table 1) One promising example is the KRAS G12C inhibitor sotorasib, which covalently binds the mutant cysteine in a hidden pocket of KRAS, traps the protein in its inactive GDP-bound state, and effectively quenches aberrant MAPK signaling in G12C-mutant colorectal tumors (129). This evidence concerns the gene KRAS and colorectal neoplasm.