Therefore, MAPK signaling, which contributes to the initiation of MM and progression to metastasis, is hyperactivated in most cases of human cutaneous MM [5], and this evidence has been applied to the development of new MM therapies using various targeted inhibitors for BRAFV600E and MAPK kinase (MEK), as well as immune-based strategies, resulting in remarkable improvements in the survival and quality of life in the past 10 years [4,6,7,8]. The gene discussed is MAP2K7; the disease is Miyoshi myopathy.