Our results support a model wherein activation of the SQSTM1/p62-Nrf2 pathway — in concert with the PERK-eIF2α/ATF4 axis — directs reprogramming of MM cells, modulating redox and energy homeostasis via elevated FAO and inducing prosurvival autophagy involving GABARAPL1 upregulation [15, 26–29, 34–36]. The gene discussed is GABARAPL1; the disease is Miyoshi myopathy.