Recent studies reveal its oncogenic role via epigenetic silencing of tumor suppressors, thereby promoting neoplastic transformation, metastatic potential, and therapeutic recalcitrance.[49] In neurological contexts, Dnmt1 overexpression exacerbates neuronal apoptosis, while its inhibition protects motor neurons in amyotrophic lateral sclerosis (ALS) models and mitigates cerebral ischemic injury.[39] However, the functional significance of Dnmt1 in SCI and its potential regulation of Pon3 expression remain unexplored. Here, PON3 is linked to neoplasm.