As such, BAFF, when in excess, could be related to the premature development of CVD; this can either be directly—through it being overtly produced by adipocytes and acting as an adipokine linking obesity and inflammation, and by contributing to the apoptosis of endothelial cell progenitors (a process known as endothelial dysfunction, a triggering factor for atherosclerosis development)—or indirectly, by altering the atherosclerosis immune surveillance processes, which are usually warranted by Breg populations such as MZ B-cell populations [178,179]. Here, TNFSF13B is linked to atherosclerosis.