AKT1 and Miyoshi myopathy: Dysregulated PI3K signaling pathway is a frequent event in MM, including (1) increased insulin-like growth factor 1 (IGF-1) and interleukin-6, both of which promote MM cell proliferation and survival [7, 8]; (2) silenced phosphatase and tensin homolog (PTEN) that antagonizes the PI3K/AKT signaling [9]; (3) overactivated PI3K/AKT [10].