TP53 and Fanconi anemia: In MITOK overexpressing muscles, different genes implicated in cellular stress response and DNA repair were induced, including growth arrest and DNA damage-inducible 45α (GADD45a), which is upregulated by fasting and immobilization-induced atrophy [13, 14], p53 and its downstream target p21, both involved in muscle atrophy [15, 16], and FANCL, one of the genes of the Fanconi Anemia (FA) family, required for the activation of the FA pathway, that is involved in DNA repair [17] (Fig. 4I).