The p16−/− lesion accelerates the onset of UVR-induced melanomas in HGF mice while retaining melanoma frequency and low metastatic activity.11 Mouse strains harbouring selective inactivation of either Nme1 (Nme1Δ/Δ)8 or Nme2 (Nme2Δ/Δ)9 (Fig. 1a) were crossed with HP mice, yielding the strains HGF: P16−/−: Nme1Δ/Δ (“HPN1”) and HGF: P16−/−: Nme2Δ/Δ (“HPN2”), respectively (Fig. 1b). This evidence concerns the gene NME1 and melanoma.