Additionally, high frequency stimulation inhibited IκB-α (an NF-κB cytoplasmic inhibitor protein) deterioration and hindered TNF-α-prompted NF-κB activation and p65 nuclear translocation, supporting an anti-inflammatory role for high frequency stimulation (HFS) in astrocytes in a PD rat model (Campos et al., 2020). This evidence concerns the gene NFKB1 and Parkinson disease.