Most critically, our computational predictions including the proposed ceRNA interactions and the role of SEMA6A require experimental validation: the inferred ceRNA interactions (e.g., XIST - miR-155-5p - CD4 axis) need verification through luciferase reporter assays and RNA pulldown experiments; putative epigenetic mechanisms like XIST-mediated H3K27me3 deposition at CD4 regulatory elements remain unexamined in PD-relevant contexts; and causal links between CD4 dysregulation and immune dysfunction (e.g., Th17 polarization) await confirmation in primary T-cell models. The gene discussed is CD4; the disease is Parkinson disease.