In breast cancer development, up-regulation of the KRAS/MAPK signaling can occur through multiple facets, and it has been shown to be increased in many breast cancer samples either by over-expression of growth-factor-receptor tyrosine kinases primarily HER2/ErbB-2, EGFR, and IGFR or by activating mutations [22], [23], [24], [25]. The gene discussed is KRAS; the disease is breast carcinoma.