INS and type 1 diabetes mellitus: Our study suggests that the selective modulation of MECL1 (encoded by PSMB10) using selective cell-permeable inhibitors of the trypsin-like site [47] may be beneficial to reduce beta cell immunogenicity and the T cell response mounted against the INS-DRiP peptide to limit type 1 diabetes progression, shedding new light on the role of the immunoproteasome, rather than the constitutive proteasome, as an important player in beta cell immunogenicity.