The study of miR-211 in melanotic melanoma cells has allowed us to demonstrate that it is part of the “normalization program” triggered by the inhibition of the ERK pathway: the consequent derepression of MITF promotes not only a switch from glycolysis to oxidative phosphorylation through PGC1alpha and mitochondrial biogenesis [3, 69], but also a more differentiated phenotype through TRPM1/miR-211 and the melanin biosynthetic pathway. The gene discussed is PPARGC1A; the disease is melanoma.