Future investigations should also be aimed to identify whether (1); endogenous C4BP is protective by comparing inducible NLRP3 inflammasome-driven disease progression in WT and C4bp-/- mice (e.g. collagen-induced arthritis or silicosis), and (2) whether injected recombinant C4BP is protective in inflammasome-driven mouse disease models, such as the APP/PS1 Alzheimer’s disease model (56). The gene discussed is APP; the disease is silicosis.