Therefore, based on the above and considering that ALS and AD, as well as other neurodegenerative diseases, share common mechanisms for the accumulation of misfolded molecules at the mitochondrial level, we can hypothesize that, by binding VDAC1, NHK1 competes with Aβ oligomers for the same binding site, thus preventing mitochondrial dysfunction. The gene discussed is VDAC1; the disease is neurodegenerative disease.