The expression levels of PI3K and PDK1 (both upstream of SGK3 and Akt), and p-SGK3 proteins increased, while the expressions of Akt and p-Akt proteins did not change, suggesting that C3a promoted the formation, differentiation, and functioning of osteoclasts in MM patients by regulating the PI3K/PDK1/SGK3 pathway. The gene discussed is PDK1; the disease is Miyoshi myopathy.