TLR2 levels were increased in postmortem brain samples of PD patients, the TLR2 agonist PAM3CSK4 increased the levels of endogenous α-synuclein in vitro and in transgenic mice, while blocking TLR2 receptors with antibodies enhanced α-synuclein clearance [295] and blocked neuron-to-neuron and neuron-to-astrocyte α-synuclein transmission which promoted NF-κB-dependent pro-inflammatory responses [296]. The gene discussed is NFKB1; the disease is Parkinson disease.