GLI1, can be phosphorylated by cAMP-dependent protein kinase (PKA), casein kinase I (CKI) and GSK3β, which in turn results in β-TRCP-mediated protein degradation by the ubiquitin-proteasome system [46], [47], which provides us a direction by targeting GLI1 on PDA therapy. This evidence concerns the gene GSK3B and Patent ductus arteriosus.