Oxidative stress stands as a primary contributor to autism pathogenesis, precipitating: (1) mitochondrial dysfunction in CNS cells coupled with heightened lipid peroxidation, protein oxidation, and DNA damage; (2) inciting neuronal inflammation, initiating cerebral plaque formation, fostering aberrant neuronal growth, and releasing detrimental pro‐inflammatory cytokines; (3) triggering immune responses; and (4) inhibiting methionine synthase, which leads to epigenetic perturbations via diminished DNA methylation, ultimately disrupting brain development (Bjørklund et al. This evidence concerns the gene MTR and autism.