OGT‐mediated protein O‐GlcNAcylation causes the inhibition of a nuclear ubiquitin‐proteasome system, which is responsible for serum response factor stabilization and Krüppel‐like factor‐4 repression in vascular smooth muscle differentiation in aneurysm and injury‐induced neointimal hyperplasia.[34] Our study illustrated that T‐2 toxin stimulation reduced β‐arrestin‐1 ubiquitination and its binding with MIB1 in podocytes and glomeruli of mice. This evidence concerns the gene OGT and aneurysm.