Thus, because of canonical TrkB.FL neuroprotective effect (Reichardt, 2006; Akil et al., 2016), these results correlate with EOM and SOL being more resistant to neurodegenerative diseases such as ALS, suggesting that this is an advantageous molecular phenotype at the same time that these muscles benefit from a reduced truncated TrkB expression. The gene discussed is NTRK2; the disease is neurodegenerative disease.