The combination of p16INK4a deficiency with activated H-Ras (Serrano et al., 1993; Chin et al., 1997), N-Ras (Ackermann et al., 2005), and K-Ras (Monahan et al., 2010) in mouse models have been shown to promote highly penetrant melanomas with short latency. Here, KRAS is linked to melanoma.