AKT1 and Miyoshi myopathy: We found that NEDD4‐1 directly binds with Akt, and NEDD4‐1 could ubiquitinate Akt and degrade pAkt‐Ser473 via the proteasome in MM, which may be due to the K63 linkages required for Akt ubiquitination, whereas K48 linkages target pAkt‐Ser473 for proteasomal degradation.10 Since Bor and MG‐132 are both proteasome inhibitors, they are expected to lead to similar results if NEDD4‐1 promotes pAkt‐Ser473 degradation, which should be rescued by both chemicals.