Our results and previous research thus prompt the hypothesis that patients suffering from genetic diseases caused by LoF or LoE TBK1 mutations, such as amyloid lateral sclerosis (ALS) or frontotemporal dementia (46–48), may benefit from dual RIPK1 and NLRP3 inhibitor therapy to ameliorate neural and systemic inflammation, particularly during bacterial infection. Here, NLRP3 is linked to hereditary disease.