Indeed, release of IL-36γ induced by pathogenic microbes paralleled that of the cytosolic housekeeping protein GAPDH, suggesting that in the context of infection the major mechanism of IL-36γ release may be a result of pathogen-induced membrane damage or necrosis rather than through an active response to microbial challenge, perhaps similarly to IL-33 and IL-1α. Here, IL1A is linked to infection.