Oxidative stress, accumulation of aggregated and misfolded protein aggregates, and neuroinflammation have been suggested to play roles in the pathogenesis of Parkinson’s disease (PD) [1, 2] These factors impair the ubiquitin-proteasome system (UPS) which is critical for protein metabolic homeostasis [3–5], and they promote the replacement of constitutive proteasome subunits β1, β2 and β5 by the respective immunoproteasome catalytic subunits β1i/ low-molecular-mass protein 2 (LMP2, PSMB9), β2i/multicatalytic endo- peptidase complex-like 1 (MECL1, PSMB10) and β5i (LMP7, PSMB8) [6–8]. Here, PSMB9 is linked to Parkinson disease.