Long-term exposure to TNF-α led to hyperplasia of the lining layer, an altered macrophage phenotype, and an increase in pro-inflammatory cytokines, such as TNFA, IL6, IL8, and IL1B, reassembling key features of established RA, thereby confirming previous observations by Kiener et al. [93,96]. The gene discussed is IL6; the disease is rheumatoid arthritis.