Colorectal carcinoma still remains a challenging disease due to several contributing factors: a variety of molecular transformation pathways other than the traditional APC, KRAS and tumor suppressor gene p53 mutations are implicated in CRC development [27], altered biochemical cellular metabolism of neoplastic cells, molecular heterogeneity between the primary CRC and its metastasis and the mysterious role of intra-tumoral inflammatory cellular infiltrate. The gene discussed is KRAS; the disease is colorectal carcinoma.