To determine whether the reduced atherosclerosis burden in LDLR−/−p110γ−/− mice correlated with cell proliferation defects in lesions, we performed double immunofluorescence experiments in aortic cross-sections from high-fat diet-fed mice to test whether p110γ deficiency affected macrophage and T cell in situ proliferation (as assessed by Ki67 expression). The gene discussed is LDLR; the disease is atherosclerosis.