While, as mentioned above, wild type Kras suppresses the oncogenic activity of KrasG12D, a dimerization-deficient wild-type Kras mutant did not inhibit the oncogenic effects of KrasG12D, implying that the tumor suppressive effects of the wild type Kras is exerted via formation of an unproductive dimer with KrasG12D [37]. This evidence concerns the gene KRAS and neoplasm.