Genome-wide association studies (GWAS) point to genes regulating aspects of cell division control (e.g. CDKN2A/MTAP, PLA2G6, TERT), DNA repair (e.g. PARP1, APEX1, ATM), and pigmentation (e.g. MC1R, ASIP, TYR, SLC45A2, TYR) as the main players in conferring MM risk (Gerstenblith et al., 2010; Duffy et al., 2018). This evidence concerns the gene CDKN2A and Miyoshi myopathy.