Interestingly, there was no difference in transmigrated monocytes among HRECs challenged with L-glu, D-glu + TNF-α, and montelukast (5 μM) (Figs. 6B, 6C), indicating that CysLTR1 has a central role in hyperglycemia and TNF-α–induced inflammation and endothelial activation, and montelukast associated receptor antagonism is necessary and sufficient to alleviate such effects. The gene discussed is CYSLTR1; the disease is Hyperglycemia.