Detailed mechanistic analyses support that SENP1 maintains VEGFR2 in an un-SUMOylated state, ensuring normal VEGFR2 trafficking and signalling in EC; pathological conditions such as hyperglycemia downregulate SENP1, causing VEGFR2 hyper-SUMOylation and impaired angiogenic signalling (Fig. 8. The gene discussed is SENP1; the disease is Hyperglycemia.