Saha et al. (2016) found that H2S produced by CBS in VECs stabilizes Sp1. H2S modifies the Cys68 and Cys755 sites of Sp1 through S-sulfhydration, enhancing Sp1 binding to VEGFR-2, upregulating VEGFR-2 and NRP-1 levels, and thereby improving VEGF-induced endothelial responses to treat CBS deficiency-induced dysfunction. This evidence concerns the gene KDR and homocystinuria.