KRAS and neoplasm: The difference between these KRAS subtypes can be attributed to the difference in the structure of the amino acid binding to GTP; the original glycine residue is changed to aspartic acid or valine, which alters signal activation, such as that related to Raf, ERK, and MEK, as well as changes in the tumor matrix, resulting in changes in response to treatment [16,20,21,22].