These results suggest that a failure in mitochondrial control of Ca2+ entry by SOCs could be a possible mechanism underlying the pathology of GDAP1-related CMT, although additional defects in other Ca2+ entry mechanisms, such as voltage gated Ca2+ channels, cannot be excluded, particularly those in neuromuscular junctions [167,168,169,170]. The gene discussed is GDAP1; the disease is Charcot-Marie-Tooth disease.