Mitochondrial dysfunction is a predominant feature of ALS and has been associated with multiple pathogenic pathways in ALS, with a number of ALS candidate genes implicated in mitochondrial dysfunction, e.g. TDP-43, which forms aggregates in mitochondria and causes disruption to mtDNA transcription, ATP production and calcium homeostasis.9 The function of mitochondria is utmost essential in cell survival and metabolism, which includes ATP production via oxidative phosphorylation, calcium homeostasis and lipid biosynthesis. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.