Using this chipset, we showed that: 1) inflammatory mediators and matrix-modifying enzymes, such as TNF-α, IL-1β, IL-6, IL-8, MMP-1, and TIMP-2, were upregulated in macrophage mediated-inflamed human AF cells34; 2) the kinetic characteristics of hAFs were also modulated under degenerative conditions; 3) these phenotypic and genotypic changes were mediated by NF-κB p50 translocation and activation; and 4) micro-EI stimulation inhibited these inflammatory molecules and catabolic enzymes in inflamed AF cells induced by macrophages, particularly at 200 Hz with 150 mV/mm. The gene discussed is IL1B; the disease is atrial fibrillation.