It was founded that SOCS1 was not detected in primary hepatocytes after 6 and 48 h, although the level of SOCS1 protein was not statistically significant in the treatment and control in 24 h post-treatment (p > 0.05) (Figure 5(A)); The level of SOCS1 protein in NASH primary Kupffer cells was significantly decreased (Figure 5(C)), revealing that KCs play a major role in mediating the SOCS1/TLR4/NF-κB immune-inflammatory pathway. This evidence concerns the gene NFKB1 and metabolic dysfunction-associated steatohepatitis.