Interestingly, evidence in multiple cell types, including the pancreatic beta cell, provided compelling support for the postulation that Rac1 is constitutively activated (sustained activation) under conditions of metabolic stress (chronic exposure to hyperglycemia, hyperlipidemia, and biologically active sphingolipids, such as ceramides) [62,63]. The gene discussed is RAC1; the disease is Hyperglycemia.