Thus, they discovered that TAX was able to reduce lipid accumulation and steatosis via P2X7R and NLRP3 suppression in mice with ALD, paving the way for NFLRP3-P2X7R regulation as a potential therapeutic target for alcohol-related liver steatosis [61] (Table 2), although further research is needed. The gene discussed is NLRP3; the disease is steatosis.