Studies suggest that PI3K-AKT-specific inhibitors significantly upregulate Th1 and Th17 cells in PBMCs of MG patients, and mTOR/HIF-1α activates the expression of glycolytic genes to provide energy for rapid activation of immune cells, suggesting that the PI3K/AKT signaling pathway regulates immune function in MG [38]. Here, AKT1 is linked to myasthenia gravis.