AKT1 and neoplasm: gingivalis inhibits activation of caspase-3 by activating Akt and Jak/Stat dual signaling pathways, blocking the increase of mitochondrial membrane permeability caused by caspase-3, and triggering inherent mitochondrial apoptosis.93,94 At the same time, P. gingivalis can also activate the Jak/Akt/Stat3 signaling pathway to upregulate the anti-apoptotic protein Bcl-2, the tumor formation-related gene c-Myc, and the apoptosis-inhibiting gene Survivin, inhibiting the inherent apoptosis of mitochondria and cell apoptosis.95P.