Although Peli1-abrogation did not affect atherosclerosis plaque size and cholesterol levels, Peli1 deficiency resulted in an elevation of the systemic inflammation including (1) induction of atherogenic immune cell populations—Th1 cells, CD4 L-17, and T follicular helper cells; (2) increased systemic pro-inflammatory cytokines like IL-6, TNF-a, IL-17, IL-18 and IL-12p70 as well as chemokines; (3) increased levels of circulating IgE and IgG2a. The gene discussed is IL17A; the disease is atherosclerosis.