In addition, we found that (a) the more pronounced up-regulation of CDKN2A in tumors with the KRAS mutation may suggest possibility of a better response to anti-CDKN2A therapy with Villosol in KRAS-mutant CRC; and (b) the more pronounced up-regulation of genes in the proteasome pathway in the CRC tissue especially with the KRAS mutation and MSI may suggest a potential role of a proteasome inhibitor in selected CRC patients. The gene discussed is CDKN2A; the disease is colorectal carcinoma.