Although the intervertebral disc has been identified as an immune-privileged organ with no access to systemic circulation in the past few decades (Takada et al., 2002), structural deficits in the NP and annulus fibrosus (AF) and formation of tears and clefts and, in some instances, herniation allow immune cell activation and infiltration, which enhance aggrecan and collagen degradation (Risbud and Shapiro, 2014). This evidence concerns the gene ACAN and atrial fibrillation.