Given our transcriptomic evidence for MTAP regulation of extracellular matrix organization pathways (Figure 4E, Table S19), we next assessed whether MTAP perturbation affects collagen I production—a key effector mechanism in vascular fibrosis and atherosclerotic plaque formation and a defining functional hallmark of the sustained, pathological matrix-producing phenotype that drives vascular fibrosis. The gene discussed is MTAP; the disease is fibrosis.