We previously showed that concomitant, hemizygous ablation of the tandemly arranged Nme1 and Nme2 genes (Nme1+/Δ: Nme2+/Δ) converts ultraviolet radiation (UVR)-induced melanomas to highly metastatic forms in mice engineered for overexpression of hepatocyte growth factor (HGF), but the individual contributions of Nme1 and Nme2 were not addressed.6 Herein, we assessed the individual MSG activities of Nme1 and Nme2 in UVR-induced melanoma by their selective inactivation in a refined HGF-based mouse model. This evidence concerns the gene NME2 and melanoma.