Specifically, wild type RAS of the same isoform in its GDP bound state inhibits the function of the mutated isoform whereas overexpression or stimulation of the protein products of the two non-mutated, wild type RAS genes (e.g., HRAS and NRAS in a KRAS-mutated cancer) are tumor promoting in RAS-mutated tumors (reviewed in [52]). Here, KRAS is linked to neoplasm.