To determine whether activating mutations in RAS could have contributed to tumor development in our mice, either via BRAFi-induced MAPK-dependent [14] or MAPK-independent [33,34] initiation and promotion of tumorigenesis, tumor tissues were analyzed for mutations in Hras1, Kras and Nras, all in the hotspot codons 12, 13 and 61. The gene discussed is HRAS; the disease is neoplasm.