Cysteinylglycine disulfide, a metabolite of glutathione (GSH), may accumulate in response to enhanced oxidative stress, leading to endothelial dysfunction and smooth muscle cell proliferation.[36–38] TAGLN2 may indirectly elevate cysteinylglycine disulfide levels by inhibiting GSH synthesis (e.g., via GCLC inhibition). The gene discussed is GCLC; the disease is endothelial dysfunction.