The ability of NHK1 to bind and modulate VDAC1 in a similar manner to the endogenous protein, as well as its capacity to reduce the formation of toxic VDAC1‐SOD1 mutant aggregates in ALS, has already been demonstrated in both cell‐free assays and purified mitochondria from motor neuronal‐like cells (Magrì et al. 2016). The gene discussed is VDAC1; the disease is amyotrophic lateral sclerosis.