Notably, many studies have confirmed that mutations and deletions of other resident ER proteins can also affect the biosynthesis of proinsulin and insulin and contribute to the development of DM, such as the deletion of the Hsp40-type accessory chaperones ERj4 and ERj5 of BiP or mutations of the BiP-interacting proteins proline-rich receptor-like protein kinase (PERK) and TRAP (Fritz et al., 2014; Dong et al., 2008; Harding et al., 2001; Huang et al., 2021). This evidence concerns the gene INS and diabetes mellitus.