A natural deletion of arginine in α53 of DQ2 has been demonstrated to reduce affinity for DM, explaining inefficient DM-mediated peptide exchange in T1D-associated DQ2 molecules (32, 33), further supporting the idea that inefficient DM editing may play a critical role in T1D-associated autoreactive CD4+ T cell development (32, 34). Here, TOR1A is linked to type 1 diabetes mellitus.