RIPK3 (receptor-interacting protein kinase-3) deficiency in TAMs of HCC increased fatty acid oxidation (FAO) via the ROS-caspase1-PPAR (peroxisome proliferator-activated receptor) pathway, thus playing an essential role in accumulation and M2 polarization of TAMs in the TME and accelerating HCC growth [56]. Here, PPARA is linked to hepatocellular carcinoma.