A possible explanation for these results may be that Harmine could enhance the extracellular signal-regulated kinases pathway (ERK) signaling cascade in adipocytes, decline caspase-3 gene expression, which is responsible for programmed cell death in diabetes, and inhibit the nuclear factor-kappa B (NF-κB) signaling pathway [26,53,73]. This evidence concerns the gene CASP3 and diabetes mellitus.