Despite these inherent limitations of the CCN2 bioactivity regimen used in a single time course and concentration protocol, the collective data herein indicate that inhibition of CCN2 bioactivity prevents induction of fibrosis in the NASH mouse model that was studied, implicating CCN2 as a mediator in human NASH induced by type 2 diabetes. The gene discussed is CCN2; the disease is metabolic dysfunction-associated steatohepatitis.