Similarly, P. gingivalis translocates from the oral cavity to the liver, where it accelerates MASLD progression by increasing the levels of TNF-α, Il-1β, galectin-3, and pSmad2; the number of hepatic crown-like structures (HCLSs); and the MASLD activity score.45 It upregulates multidrug resistance transporters in hepatic cancer cells while also activating JAK1/AKT/STAT3 signaling to suppress apoptosis.46,47P. gingivalis also decreases the ATP-mediated activation of P2X7 receptors on dendritic cells, which impedes the activation of the NLRP3/ASC/caspase-1 inflammasome. Here, AKT1 is linked to metabolic dysfunction-associated steatotic liver disease.