They started with 98 genes with the potential to be tumor drivers, and some of them have already been on the list of mutational drivers such as TP53; chromatin modifiers: KMT2D, CREBBP, and EP300; genes encoding for the components of the BCR, Toll-like receptor (TLR), NF-κB, or RAS pathways; other tumor-related genes also affected by genetic alterations such as KRAS, BRAF, NOTCH2, and SPEN (Notch signaling modifier); and players in the immunomodulatory pathway such as B2M, CD58, CD70, and CIITA [88]. This evidence concerns the gene KRAS and neoplasm.