For example, the G12, G13, Q61 and A146 positions of KRAS accounted for most KRAS SNVs in both common and rare scenarios (lung non-small-cell tumors: 568/586 mutations; prostate tumors: 12/17 mutations; gliomas: 11/15), and the V600E mutation accounted for the plurality of BRAF SNVs in common and rare scenarios despite each gene having dozens of known activating SNVs (52 and 71, respectively). This evidence concerns the gene KRAS and glioma.