While the generation of cell-specific IL-1α and IL-1β-deficient lines is limited, due to the recent generation of IL-1αfl/fl and IL-1βfl/fl mice, the first studies using those models have demonstrated the critical role of microglial IL-1β in the establishment of pain in the context of complex regional pain syndrome [39], while cardiomyocyte-derived IL-1α has been found not to contribute to tissue remodeling during myocardial infarction [40]. The gene discussed is IL1A; the disease is myocardial infarction.