In a high-fat diet mouse model, chronic obesity elevated FAP proliferation, adipocyte infiltration, and collagen deposition in the diaphragm, leading to contractile and respiratory dysfunction, with thrombospondin 1 identified as a key obesity-related stimulator of FAP expansion, highlighting FAPs as potential targets to prevent skeletal muscle remodeling and dysfunction in obesity [13,180,181]. The gene discussed is FAP; the disease is Obesity.