Locally produced salusin-β may also act on adjacent endothelial cells to accelerate inflammatory responses and on macrophages to induce foam cell formation.[49–51] A splicing variant was also identified in the PKD1L2 gene, which is a member of the polycystin-1 family and highly homologous to the PKD1 gene causing autosomal dominant polycystic kidney disease. The gene discussed is PKD1; the disease is autosomal dominant polycystic kidney disease.