This conclusion was based on the following observations: (1) lower serum FSTL1 levels were predictive of calcific AS events, (2) decreased FSTL1 protein expression in human VICs was associated with valve calcification, and (3) FSTL1 inhibited osteoblastic differentiation of VICs partly through the downregulation of the ERK1/2 pathway. The gene discussed is FSTL1; the disease is aortic stenosis.