For example, in NAFLD the excessively activated inflammation is caused by M1 polarized macrophages.[36] In acute liver injury, KCs exhibit higher M1 polarization levels.[37] On the other side, the activation of NLRP3 inflammasomes is common in NFALD.[38] NLRP3 inflammasomes is also plays an important role in ischemia-reperfusion injury.[39] In a word, the inflammation state of the liver is inseparable from polarization and NLRP3 inflammasomes of liver macrophages. This evidence concerns the gene NLRP3 and metabolic dysfunction-associated steatotic liver disease.