Maass et al. [10] reported that missense mutations in PDE3A increase PKA-induced PDE3A phosphorylation and cAMP hydrolytic activity, causing hypertension and brachydactyly type E. In addition, several studies suggest that the intergenic regions of hPDE3A may be useful drug targets to improve anti-TNF therapy in rheumatoid arthritis, HDL cholesterol levels, and type 2 diabetes mellitus [11,12]. This evidence concerns the gene PDE3A and brachydactyly type E.