In support of the causative role of ALCAT1 in the pathogenesis of neurodegenerative diseases, ALCAT1 deficiency or inhibition not only prevented MPTP induced Parkinson’s disease but also significantly attenuated the aggregation of α-synuclein, leading to significant improvement in mitochondrial morphology, respiration, and oxidative stress in the brains of a mouse model of Parkinson’s disease [38]. The gene discussed is LCLAT1; the disease is Parkinson disease.