These findings, combined with the earlier discussed improved locomotor function and muscle strength following anti-CCN2 therapy in a murine model of amyotrophic lateral sclerosis [63] and Mdx mouse studies [64,65] in conjunction with reduced muscle fibrosis, implicate soft tissue fibrosis and degeneration as key contributors to functional declines, and anti-CCN2 therapy as a means to improve tissue function in these instances. This evidence concerns the gene CCN2 and amyotrophic lateral sclerosis.