The loss of SYNJ2BP exacerbates MAMs damage and inhibits the formation of the NLRX1–SLC39A7 complex, potentially reducing the localization of SLC39A7 in the mitochondria, increasing mitochondrial zinc ion accumulation, and ultimately leading to the exacerbation of mitochondrial dysfunction, accelerated aging of NP cells, and progression of IDD [221]. The gene discussed is SLC39A7; the disease is intervertebral disk degenerative disorder.