In ALS, the interactions may be more complex, but current data suggest the possibility that dampened ERBB4 (ALS19) function could lead the upregulation of NRG1 and secondary overstimulation of other ERBB (HER) receptors; hence, clinical trials of pan-ERBB/HER inhibitors, currently in use and approved for cancer, merit investigation in ALS. This evidence concerns the gene NRG1 and amyotrophic lateral sclerosis.