Regarding inflammation, our present work shows that the typically inflammatory cytokines IL1β, IL-10, and IL-6 are present in higher levels in the sera of infarcted patients, especially in severe cases, compared to healthy and stable atherosclerotic individuals, in accordance with already published studies that suggest that the increases in these cytokines play critical roles in the activation of post-infarction inflammation, promoting matrix degradation, delayed healing of the infarcted area, and cardiomyocyte apoptosis, thus mediating post-AMI dysfunction (61–63). The gene discussed is IL6; the disease is infarction.