Of interest in this respect, there is accumulating evidence that aberrant NRG1 expression (in addition to the loss-of-function ERBB4/HER4/ALS19 mutations) may be implicated in the pathogenesis of ALS [40]; murine models have shown increased type I (secreted) NRG1 expression that could contribute to disease progression via glial cell over-stimulation in ALS. The gene discussed is ERBB4; the disease is amyotrophic lateral sclerosis.