Their findings can be generalized as follows: (a) decreased miR-18b-5p regulated Hif1α expression post-transcriptionally, (b) Hif1α increased Mef2c as a transcription factor, (c) Mef2c greatly increased miR-206 expression, (d) miR-206 degraded both mctp1 and Rarb, (e) decreased mctp1 inhibited Ca2+ signal, (f) decreased Rarb prevented neuronal cell differentiation and (g) decreased miR-18b-5p promoted apoptotic cell death in ALS SOD1 mutation. Here, MEF2C is linked to amyotrophic lateral sclerosis.