Main findings can be summarized as follows: (i) Voluntary EXE limited further ATS progression, and promoted stability of established Ang II-dependent plaques; (ii) Voluntary EXE reduced aortic VCAM-1 and ICAM-1 expression; (iii) Voluntary EXE reduced splenic expression of pro-inflammatory cytokines (IL-1β and IL-18), while increasing that of anti-inflammatory IL-4; (iv) Voluntary EXE did not modulate aortic and splenic expression of Th1/Th2, and M1/M2 polarization markers; finally, (v) Voluntary EXE reduced total plasma cholesterol level, but not blood pressure, and plasma renin activity. The gene discussed is VCAM1; the disease is Andersen-Tawil syndrome.