Despite these differences in metabolism between mice and humans, we have shown previously that the key molecular inflammatory responses in obese Ldlr−/−.Leiden mice and humans are similar (Morrison et al., 2018): the hepatic inflammatory response in NASH patients (non-alcohol steatohepatitis; due to an increased metabolic load) has large similarities to the obese Ldlr−/−.Leiden mice fed with a HFD demonstrated by the activation of the majority of identical inflammatory processes and master regulators (e.g., TNF, CSF2, TGFB1) (Morrison et al., 2018). This evidence concerns the gene CSF2 and metabolic dysfunction-associated steatohepatitis.