Aluminum particles are phagocyted by these cells (macrophages and dendritic cells), and they cause disruption of the phagolysosomes and release of active cathepsin B into the cytoplasm which may be a sufficient signal for NLPR3 (also named as NALP3) activation inflammasome, resulting in the release of active IL-1β and IL-18 [35, 36], and this is also a well-known pathogenic mechanism in silicosis [37, 38]. The gene discussed is IL1B; the disease is silicosis.