For example, in the treatment of nonalcoholic steatohepatitis, self‐protection is mainly through IL‐10 secretion by M2‐like macrophages, while in stroke, it is mainly through elevated CCR5 expression and chemotactic DNT infiltration into the lesion site to exert inflammatory protection [12, 38]. This evidence concerns the gene CCR5 and metabolic dysfunction-associated steatohepatitis.