CCL3 and heart failure: Other data showed that circulating monocytes of patients with heart failure carrying DNMT3A mutations demonstrated a pro-inflammatory transcriptome with significantly increased expression of inflammatory genes compared with monocytes derived from patients with heart failure without DNMT3A mutations, especially inflammatory interleukin IL-1β, IL6, IL8, the inflammasome NLRP3, and the macrophage inflammatory proteins CCL3, CCL4, and resistin, of which the latter mediates monocyte-endothelial adhesion and may all together contribute to an aggravation of chronic heart failure [65].