Examination of upstream regulators based on the differential gene expression data revealed a predicted activation of TGF-β1 in Crtap-/- mice and predicted inhibition of dystrophin (DMD) along with several for which activation state was unclear, including platelet-derived growth factor-BB (PDGF-BB), β-catenin (CTNNB1), and tumor necrosis factor (TNF) (Figure 6C). Here, CRTAP is linked to Duchenne muscular dystrophy.