Regarding the mechanism, ZIP4 downregulated the HDAC4-FoxO3a pathway; HDAC4 overexpression abated the damage-boosting function of ZIP4 overexpression in the ex vivo IDD model; FoxO3a knockdown offset the damage-promoting function of ZIP4 in the in vitro IDD model. The gene discussed is HDAC4; the disease is intervertebral disk degenerative disorder.