Recent studies underscore the therapeutic importance of these pathways: PI3K/AKT/mTOR signaling, activated by IL-6 and IGF-1, supports MM cell growth and resistance, and its inhibition—using agents like mTOR inhibitors, temsirolimus [84], everolimus [85]; or AKT inhibitors, afuresertib [86] or resibufogenin [87]—show promise in relapsed/refractory settings [83]. The gene discussed is AKT1; the disease is Miyoshi myopathy.