To explore the role of individual components of the Cdkn2a locus by comparing models in which Cdkn2a (including p19Arf) were disrupted with or without concomitant loss of Cdkn2b Badhai et al. showed that the additional disruption of Cdkn2b further added to the aggressiveness of the resulting MMs, providing also an explanation for the predominance of deletion of the complete CDKN2A-CDKN2B locus in human MM over point mutations in CDKN2A (Badhai et al., submitted). The gene discussed is CDKN2A; the disease is Miyoshi myopathy.