β‐arrestin‐2 mediates Nephrin endocytosis along with injured slit diaphragm integrity through interaction with the Nephrin C terminus in streptozotocin‐induced hyperglycemia mice.[29] As a molecular scaffold, β‐arrestin‐1 recruits CXCR4 and Src to generate a CXCR4/β‐arrestin‐1/Src signaling body, inducing podocyte injury in an adriamycin‐induced mouse model of nephropathy.[13b] Herein, we determined that β‐arrestin‐1, rather than β‐arrestin‐2, mediated T‐2 toxin‐induced glomerular podocyte injury. Here, SRC is linked to Hyperglycemia.