Erk1/2 and P38 indirectly act on AP-1, while P38 and JNK indirectly act on NF-κB. It directly acts on VEGF, McP-1, TNF-α, IL-6, IL-1, and IL-8 genes, and ultimately indirectly improves angiogenesis, inflammation, and atherosclerosis (shown in Figure 13). The gene discussed is NFKB1; the disease is atherosclerosis.