Nicotinamide mononucleotide (NMN), a precursor of nicotinamide adenine dinucleotide important for the maintenance of redox homeostasis, increased the expression of SIRT1 and SIRT6 as well as SOD activity in cultured rat tenocytes and Achilles’ tendons with collagenase-induced tendinopathy, but decreased the levels of NOX1, NOX4, IL6, ROS, and apoptosis demonstrating the antioxidative effects of NMN [37]. The gene discussed is SOD1; the disease is disease of the tendon.