Figure 1 demonstrates a model whereby HIV-1 infection can stimulate the NLRP3 inflammasome to result in IL-1β secretion which impacts on various cell types including endothelial cells, macrophages, monocytes, and smooth muscle, signaling through soluble factors including chemokines, cytokines, adhesion molecules, matrix metalloproteinases to result in progression of atherosclerotic disease. The gene discussed is IL1B; the disease is HIV-1 infection.