Under ischemic and high-fat diet (HFD) loads, CTSS participates in cardiovascular remodeling and the formation of atherosclerosis by mediating transforming growth factor-beta (TGF-β) and peroxisome proliferator- activated receptor gamma (PPAR-γ) or activating the p38 mitogen-activated protein kinase (MAPK) pathway [25–27]. The gene discussed is PPARG; the disease is atherosclerosis.