As our study found that the main reason for GA50 to activate the NLRP3 inflammasome of HMC3 cells is its interaction with SQOR, we hope to establish a feasible method to reverse the pathological progression of C9-ALS by disrupting the interaction between GA50 and SQOR, such as finding small molecule inhibitors. The gene discussed is NLRP3; the disease is amyotrophic lateral sclerosis.