Whilst activation of both KRAS and B-RAF can stimulate downstream ERK activation, its aberrant activation is not necessarily solely reliant on B-RAF or KRAS mutations, since ERK activity was seen to be not significantly different between WT or mutated B-RAF or KRAS in melanoma, and other ERK regulatory mechanisms are thought to be involved (Houben et al., 2008). The gene discussed is BRAF; the disease is melanoma.