This highlights the pivotal role of mTORC1 in mediating pro‐oxidant and pro‐inflammatory effects of BCAA on ECs, and it might be in agreement with the role of the overactivation of Akt‐mTORC1 axis and the progression of the metabolic syndrome, future development of T2DM and the associated endothelial cell activation and endothelial dysfunction.37, 38, 39 The molecular mechanisms responsible for the mTOR‐dependent activation of NOX and NF‐κB in response to BCAA are unknown and this is a limitation of our study. The gene discussed is NFKB1; the disease is endothelial dysfunction.