NF-κB-mediated inflammation induces LUM production by cardiac fibroblasts, and increased LUM promotes raised levels of TGF-β1, exacerbates fibrosis in cardiac fibroblasts and promotes cell adhesion through the TGF-β2/Smad 2 signaling cascade promoting cell adhesion, which in turn exacerbates HF.[23,24] The osteopontin is an effector of extracellular signals that induces and maintains the growth and fibrosis of cardiomyocytes. The gene discussed is LUM; the disease is hydrops fetalis.