IL-1β and IL-1α, together termed IL-1, could promote innate immunity by inducing CXC- and CCL- chemokines (e.g., IL-8) for neutrophil recruitment (99–101), directly [e.g., in myocardial infarction (102)] or indirectly [e.g., by enhancing TH17 cell differentiation (103–105)] upregulating granulopoiesis and mature neutrophil release from the bone marrow, increasing the formation of neutrophil extracellular traps (NETs) for the trapping and killing of bacteria (106–108), and driving M1/M2 polarization and macrophage activation (109–111). Here, IL1A is linked to myocardial infarction.