In addition, the inhibition of NAD+-degrading enzymes (e.g., poly ADP-ribose polymerase (PARP), cluster of differentiation 38 (CD38), and selective androgen receptor modulators (SARMs)) increases the tissue intracellular NAD+ content, and supplementation with NAD+ precursors (e.g., β-nicotinamide mononucleotide (NMN), nicotinamide riboside, etc.)also significantly elevates myocardial NAD+ levels to ameliorate heart failure. This evidence concerns the gene CD38 and heart failure.