Besides the gain-of-function mutations in the gene, KRAS amplification is also found in 1 out of 5 patients with testicular germ cell tumor or ovarian cancer; notwithstanding, the high prevalence of the gene amplification may result from different types of molecular machinery, as the TGCTs have the genetic nature of chromosome 12 amplification [30], while the prevalent TP53 deficiency in OVs can lead to a tolerance of increased gene load [31]. This evidence concerns the gene TP53 and ovarian carcinoma.