Enhanced expression of pro-inflammatory cytokines (Interleukin-1β [IL-1β] and tumor necrosis factor-α [TNF-α]) found in degenerated human IVDs induces progressive degradation of major extracellular matrix components by stimulating matrix-degrading enzymes [4] that induce disc ruptures, including several types of AF tears [5,6,7]. The gene discussed is TNF; the disease is atrial fibrillation.