As anti-inflammatory therapies focused at restraining the hyperactivation of the innate arm of the immune system, demonstrated anti-atherosclerotic Volume 5, Issue 5 171 efficacy (e.g., Canakinumab, the antibody against Il-1β [50]) or reached clinical approval or the reduction of cardiovascular risk (as it is the case of Colchicine [51]), identifying strategies to control neutrophil aging without altering their efficacy against infection might help to improve the therapeutic options towards cardioimmunometabolic co-morbidities (Figure 1). This evidence concerns the gene IL1B and infection.