Subpopulations of FAPs are dysregulated in many NMDs and accumulate within atrophied ALS mouse muscles (Gonzalez et al., 2017), exhibit varied gene signatures in response to denervation and cardiotoxin injury (Madaro et al., 2018), and activate IL-6-STAT3 signaling in response to denervation that may lead to fibrosis related to NMDs (Madaro et al., 2018). This evidence concerns the gene STAT3 and amyotrophic lateral sclerosis.