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. Here, KRAS is linked to neoplasm.