Thus, it is conceivable that excess oxidative stress during AKI suppresses GSK3β inhibitory phosphorylation at serine 9 and augments GSK3β kinase activity, leading to GSK3β accumulation due to reduced ubiquitination and degradation, which promotes GSK3β overactivity, further impairs Nrf2 antioxidant response and exacerbates oxidative injury, resulting in a vicious cycle that drives progressive transition of AKI to CKD. The gene discussed is GSK3B; the disease is acute kidney injury.