NSC34 cells stably expressing WT or G93A hSOD1 were a gift from Dr. Manfredi (Weill Medical College of Cornell University, USA). NSC34 were maintained in DMEM supplemented with 10% v/v FBS and 1% (v/v) penicillin/streptomycin. For differentiation, cells were plated onto poly‐d‐lysine‐coated plates and grown in differentiation medium, containing 1:1 DMEM/Ham's F12 supplemented with 1% FBS, 1% P/S, and 1% modified Eagle's medium non‐essential amino acids. ALS patient‐derived fibroblasts (ALS 1: ND29509; ALS 2: ND30327; ALS 3: ND32969) and fibroblasts of control healthy individuals (H1:AG07123; H2:AG04146) were purchased from Coriell Institute, USA. All fibroblast cultures were maintained in MEM supplemented with 15% (v/v) FBS and 1% (v/v) penicillin/streptomycin at 37°C in 5% CO2‐95% air. NSC34 cells were treated with P110, vehicle (TAT47–57) at a final concentration of 1 μM every 24 h in serum‐free media. Similarly, for patient‐derived fibroblasts, TAT or P110 peptides were added once daily for the duration of the experiment at 1 μM final concentration. All experiments were carried out in defined serum‐free media. Cells with fewer than 18 passages were used in all experiments. It should be noted that fibroblasts from healthy subjects used in previous studies (Guo et al, 2013; Qi et al, 2013) all showed similar mitochondrial morphology and functions and these parameters were unaffected by P110 treatment of these control cells. Further, 5‐month P110 treatment is without adverse effects, including motor functions and mitochondrial dynamics. Therefore, P110 effects are specific for pathological and not physiological fission.