Upregulation of CD38 in patients with SSc, resulting from its induction by cytokines such as TGF-ß, IL-6 and senescent cell-derived SASP enriched in the fibrotic tissue microenvironment, will promote NAD+ consumption and decline, which in turn impairs the function of sirtuins and other NAD+-dependent cellular enzymes. Here, IL6 is linked to systemic sclerosis.