Downregulation of OGT through pharmacological or genetic interventions is sufficient to prevent proliferation of human gastric tumor cells, NUGC‐3, and HEK293 in vitro, and relieve renal dysfunction and podocyte shedding in diabetic mice and patients with diabetic nephropathy.[37] In the current study, our results showed that insufficient OGT alleviated glomerular abnormalities and proteinuria in T‐2 toxin‐stimulated mice. Here, OGT is linked to gastric neoplasm.