CCN2 and diabetes mellitus: Accordingly, in diabetic mice, C66 has been shown to reduce the diabetes-associated increase in p300/CBP expression and HATs activation by JNK inactivation, whereby the subsequent histone hyper-acetylation causes specific increase in p300/CBP-mediated accumulation of CTGF, PAI-1, and FN-1 gene promotors (Fig. 6).