Evidence indicated that, although mice genetically lacking miR-206 were able to engage normal neuromuscular synapses during development, deficiency of miR-206 in the ALS mouse model accelerates the disease progression, at least in part through the histone deacetylase 4 (HDAC4) and fibroblast growth factor signaling pathways (Figure 2) [78]. The gene discussed is HDAC4; the disease is amyotrophic lateral sclerosis.