Interestingly, in contrast to the dual peroxisomal and mitochondrial fission defect observed in skin fibroblasts from patients with DNM1L or MFF mutations [167,168,169,170,171], the currently identified missense disease mutants of GDAP1 appear to impair only mitochondrial fragmentation in mouse neuroblastoma N1E-115 cells (loss of GDAP1 also leads to peroxisomal elongation) [47]. This evidence concerns the gene GDAP1 and neuroblastoma.