Conversely, arguments for GDF‐15 as a surrogate biomarker showing a compensatory increase with disease severity yet without negative effects can be found in preclinical models of metabolic dysfunction‐associated steatohepatitis [22] and toxin‐induced liver disease [21, 41], where GDF‐15 knockout led to a worsening of hepatic steatosis, inflammation, and fibrosis, while recombinant GDF‐15 [21] treatment or GDF‐15 overexpression [22, 41] attenuated it. The gene discussed is GDF15; the disease is liver disorder.