Aspects to be further explored include: 1) tissue-specific differences in the benefits provided by NAD re-equilibration in the context of telomere shortening/dysfunction; 2) the molecular pathways linking telomere shortening/dysfunction and dysregulated NAD consuming enzymes, e.g., CD38 hyperactivation; 3) Is CD38 hyperactivation responsible for telomere shortening/dysfunction-mediated pathophysiology in other short telomere syndromes and animal models? Here, CD38 is linked to telomere syndrome.