ACO2 and hereditary neurological disease: Although the expression levels of these proteins were only evaluated in leukocytes, considering the ubiquitous expression characteristics of these two proteins, and the previous successful cases of identifying neurogenetic diseases using transcriptome data from leukocyte samples (Rentas et al., 2020), it suggests the possibility that these two proteins may serve as key mediator molecules in the development of neural atrophy caused by ACO2 mutations.