Given that impairments in Ca2+ homeostasis have been documented in patients with neurodegenerative diseases such as AD [44], PD [45], and Huntington’s disease (HD) [46], and considering that neurons from MICU1 knockout (KO) mice and MICU1-deficient patient-derived cells exhibit increased susceptibility to mitochondrial Ca2+ overload, excitotoxicity, and cell death [47], it is warranted to further investigate whether the SIRT1-regulated pathway of mitochondrial calcium uptake via MICU1 plays a role in neuronal secondary injury or death in these conditions. The gene discussed is SIRT1; the disease is Huntington disease.