As expected, CDAA-HFD led to a reduction in body weight and induced a MASH phenotype, as evidenced by increased plasma levels of alanine and aspartate aminotransferase (ALT and AST, respectively), increased liver weight, steatosis, picrosirius red (PSR) positive fibrosis area, and CD45+ immune cell infiltrates (Figure 5B–H). The gene discussed is PTPRC; the disease is steatosis.