Moreover, as shown in Figure 7H–K and Figure S7B–E (Supporting Information), administration of GCA increased the levels of IL1β, IL‐6, and TNFα, which have been previously reported to increase lipid accumulation and cell death, causing steatosis and inflammation on hepatocytes.[25] However, TLR9 blockage blunted the functional role of GCA(Figure 7H–K; Figure S7B–E, Supporting Information). The gene discussed is IL6; the disease is steatosis.