This is reflected in mouse models, where melanocyte-specific activation of BRAF or NRAS is insufficient to generate melanomas but can do so when combined with loss of INK4a by mutation (Ackermann et al. 2005; Dhomen et al. 2009; Goel et al. 2009; Burd et al. 2014; Damsky et al. 2015) or its silencing by activated β-catenin (Delmas et al. 2007). The gene discussed is NRAS; the disease is melanoma.