(217) reported that macrophages from lupus-susceptible MRL/lpr mice failed to mature lysosomes, thereby promoting the accumulation of IgG immune complexes (IgG-ICs) containing apoptotic debris, which would promote phagolysosomal membrane permeabilization, allow leakage of dsDNA into the cytoplasm, activate AIM2, and trigger the assembly of inflammasome. Here, AIM2 is linked to systemic lupus erythematosus.