Since the blockade of the P2X7 receptor in experimental animals (via P2X7 receptor gene deletion or using pharmacological agents) results in reduced fat accumulation in the liver, reduced NLRP3 activation and IL-1β production and release, reduced inflammation, reduced liver steatosis evolution to NASH, and reduced liver fibrosis, it is possible to hypothesize that the P2X7 receptor/NLRP3 axis might be an effective therapeutical target to tackle liver steatosis and the fibrotic evolution of NASH [38]. The gene discussed is NLRP3; the disease is metabolic dysfunction-associated steatohepatitis.