This reduces SWELL1 degradation and enhances the passage of SWELL1-LRRC8 heteromers through the ER and Golgi apparatus to the plasma membrane—thereby rectifying the SWELL1-deficient state in multiple metabolically important tissues in the setting of metabolic syndrome to improve glycemic control via both insulin sensitization24,25,30 and secretion28,29 mechanisms. The gene discussed is LRRC8A; the disease is metabolic syndrome.