Consistently, Tat treatment also increased the lesional areas at the brachiocephalic artery (BCA) of IKKβF/FLDLR−/− mice by 320.2% (Figure 2B, 10448.8 ± 1746.0μm2 vs. 2486.6 ± 377.6μm2) but deficiency of myeloid IKKβ abolished the impact of Tat proteins on atherosclerosis development in the BCA of IKKβΔMyeLDLR−/− mice (Figure 2B, 4940.9 ± 1520.5μm2 vs. 3777.7 ± 997.4μm2). The gene discussed is IKBKB; the disease is atherosclerosis.