The cardioprotective mechanism of nobiletin included the suppression of NADPH oxidase-mediated ROS production and downregulated the expression of transforming growth factor- (TGF-) β1, fibronectin, collagen, JNK, P38, and NF-κB. Therefore, nobiletin was able to inhibit NF-κB activation and mitigate fibrosis in the diabetic mouse heart [141]. This evidence concerns the gene NFKB1 and benign neoplasm.