AKT1 and thyroiditis: In mouse in vivo and in vitro models of thyroiditis, an increased miR-125a expression reduces autophagy and cell proliferation and increases the apoptotic rate and the expression of proinflammatory factors tumor necrosis factor-α, IL-1β, IL-6, and IL-18 via downregulation of the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR)signaling pathway [32].