The Ldlr−/−.Leiden model for instance, while mimicking many aspects of human NASH (e.g., pathophysiology, histology, underlying molecular processes; Liang et al., 2014; Morrison et al., 2016; Mulder et al., 2016; van Koppen et al., 2018), is unsuitable to study interventions that require a functioning LDL receptor (Zimmer et al., 2017). This evidence concerns the gene LDLR and metabolic dysfunction-associated steatohepatitis.