To understand the role of endogenous TLR4 in mediating the LPS-induced PKCδ activation in NASH, we examined the TGF β1, α-SMA expression and PKCδ activation in response to LPS from mice that carry a spontaneous mutation in TLR4 (Tlr4Lps-d) [15]. The gene discussed is ACTA1; the disease is metabolic dysfunction-associated steatohepatitis.