Likhitpanichkul et al. [37] further evaluated the role of inflammation in matrix homeostasis and the mechanoresponse of AF cells subjected to CTS, showing that the concomitant exposure of AF cells to TNF-α and pathological strains determined increased IL-1β and IL-8 production and a modified AF cytoskeleton. The gene discussed is IL1B; the disease is atrial fibrillation.