In the context of ALS, aggregates of mutant variants of SOD1 have been observed to accumulate on the OMM through direct interactions with VDAC1 (Israelson et al., 2010) and Bcl-2 (Pedrini et al., 2010), causing VDAC dysfunction leading to altered membrane potential, morphology and protein trafficking in mitochondria. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.