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. This evidence concerns the gene CCN2 and type 2 diabetes mellitus.