Several pro-fibrotic genes were downregulated, including: VCAN (Versican) (61); LUM (Lumican), an ECM-localized proteoglycan that binds collagen and is important for fibrosis, is associated with inflammation, and is increased in experimental and clinical heart failure (62); SERPINE2, which is increased in pressure overload- and angiotensin II-induced cardiac remodeling downstream of ERK1/2 signaling and increases collagen deposition (63); and the integrin ITGA6, associated with collagen deposition (64). The gene discussed is MAPK3; the disease is heart failure.