These observations are consistent with those of previous studies reporting that high levels of pAkt‐Ser473 activation may promote cell proliferation and that low levels of pAkt‐Ser473 activation cause cell growth inhibition.46 Furthermore, the intracellular Akt signaling pathway is reportedly significant in modulating a vast array of cellular processes involved in the cell cycle and apoptosis.47, 48 The actions of NEDD4‐1, as a tumor suppressor gene, may have consequences in MM due to the ubiquitination of Akt and a decrease in Akt phosphorylation. This evidence concerns the gene AKT1 and Miyoshi myopathy.