As inflammasome-mediated caspase-1 activation by certain toxins is known to cause truncation and aggregation of α-synuclein in BE(2)-M17 PD cell model [55], α-synuclein fibrils may initially work like a stimulator or ROS producer that activates NLRP1 inflammasome and IL-1β, which would then further lead to increased α-synuclein aggregates and neurotoxicity in a vicious cycle manner, all of which can be mitigated by LM-021 and NC009-1 in the present study (Figures 4–6). This evidence concerns the gene CASP1 and Parkinson disease.