reported that the KRASG13X is more sensitive to GTP hydrolysis stimulated by NF1 (a GAP) than G12 mutants and Q61 mutants and partially dependent on upstream signaling from epidermal growth factor receptor (EGFR) or other RTK, which may enable EGFR inhibitors to prevent the development of colorectal cancer (CRC) with G13D mutation.91 Here, EGFR is linked to colorectal cancer.