Besides, deficiency of HDAC5 in endothelial cells of patients with Scleroderma increases FSTL1 expression and improves the ability of endothelial cells to form tubules in Matrigel, suggesting that FSTL1-mediated promotion of angiogenesis is dependent on HDAC5 (Tsou et al., 2016). The gene discussed is HDAC5; the disease is scleroderma.