The low-grade inflammation observed in the spontaneous atherosclerosis model used for our studies, with no significant differences in plasma levels of the pro-inflammatory cytokines TNFα and IL6 between the ApoE3*Leiden and ApoE3*LeidenxPCAF−/− mice, may explain why PCAF deficiency did not result in smaller lesion size, as seen in the high inflammation grade post-interventional lesions, but rather in increased lesion size due to a reduction in Tregs in the ApoE3*LeidenxPCAF−/− mice. The gene discussed is KAT2B; the disease is atherosclerosis.