The elevated K48‐linked ubiquitination and degradation of pAkt‐Ser473 that we observed upon NEDD4‐1 OE prompted us to investigate whether the change in drug sensitivity induced by NEDD4‐1 could be blocked by the Akt inhibitor Afu or the Akt upstream mediator insulin‐like growth factor‐1 (IGF‐I).23, 32 First, we evaluated the effects of Afu and IGF‐I on pAkt‐Ser473 levels in MM cells (Supporting Information Fig. S5a). The gene discussed is AKT1; the disease is Miyoshi myopathy.