The atheroprotective effect of disrupted BAFF-BAFFR signaling has been attributed to depletion of conventional proatherogenic B-2 cells.8,9 We show here that soluble BAFF also has the capacity to affect atherosclerosis beyond changes in BAFFR signaling and B cell immunity, as atherosclerotic mice treated with the anti-BAFF neutralizing Ab display a similar reduction in mature B cells and circulating Ig levels, yet they develop increased atherosclerosis. Here, TNFRSF13C is linked to atherosclerosis.