Based on these relationships between disc degeneration, senescence, and STING, we first investigated if, in the absence of a traumatic mechanical injury, activation of STING in the intervertebral disc would promote SASP and a degenerative phenotype and secondly whether the absence of STING would be protective to the intervertebral disc by delaying the SASP program and reducing the prevalence of age-related degeneration in mice. The gene discussed is STING1; the disease is intervertebral disk degenerative disorder.