More specifically, in mouse models of liver cancer, it was reported that a complex interaction involving agrin, LDL receptor-related protein 4 (Lrp4), β1 integrin, and focal adhesion kinase (FAK) mediates the adhesion of endothelial cells to cancer cells, thus promoting the sprouting of new microvessels, and that depletion of this proteoglycan results in suppressed tumor growth and metastasis to the lungs [118]. The gene discussed is LRP4; the disease is neoplasm.