CCN2 and amyotrophic lateral sclerosis: Remarkably, YAP is upregulated in dystrophic mdx muscle, denervated muscle, and in hind-limbs from the SOD1G93A ALS model [122,128], then it is possible that YAP/TEAD can be contributing to CCN2/CTGF upregulation in fibrotic skeletal muscle, in a direct way and by crosstalking with TGF-β, LPA and hypoxia/vasculogenesis pathways.