Considering that the stress-inducible cellular protein p62 serves as a selective autophagy receptor for recruitment to the lysosome and implicates in the oxidative stress response with regard to mTORC1 activation, we can hypothesize that the increased accumulation of p62 detected by us in PBMC of PD patients may happen due to disturbance of the upstream p62-regulating pathways. This evidence concerns the gene SQSTM1 and Parkinson disease.