However, our experimental data do not support this hypothesis because: (i) The microglia distribution and the cytokines levels did not experience major changes between Coq9R239X mice and Coq9R239X mice treated with β‐RA; (ii) β‐RA did not reduce iNOS expression or cytokines release in RAW cells stimulated with LPS; (iii) β‐RA did not have therapeutic effects in pharmacological or genetic models of neuroinflammation, e.g., the MPTP‐induced zebrafish model of Parkinson disease and the Ndufs4 mouse model of Leigh syndrome; and (iv) β‐RA did not inhibit mTORC1 in vivo. Here, NDUFS4 is linked to Parkinson disease.