(Wang et al., 2017; Das et al., 2018; Liu et al., 2019)], which, in turn, induce CD38 mRNA and protein expression, and stimulate activity of this NADase in adjacent non-senescent cells, including populations of macrophages and endothelia [supported by experiments described in Parikh et al., 2019], with the resultant depletion of NAD+ contributing to accelerated aging observed in COPD patients (Triest et al., 2019), and to further increase in TWEAK/TNFRSF12A signaling. This evidence concerns the gene TNFRSF12A and chronic obstructive pulmonary disease.