NFE2L1 and Parkinson disease: Villaescusa et al. (2016) reported a significant reduction in NFE2L1 levels in the SN of postmortem PD brains, while other midbrain regions showed normal expression. This selective reduction suggests that NFE2L1 dysfunction in the SN may contribute to PD pathogenesis by exacerbating the accumulation of misfolded proteins such as α-synuclein, a hallmark of PD (Villaescusa et al., 2016). Additionally, studies by Lee et al. (2011) and Chan et al. (1998) emphasize the role of NFE2L1 in regulating oxidative stress and protein turnover in neurons, both of which are critical in PD development.