The latest study found that the proinsulin in the islets of WFS1-deficient mice accumulates abnormally in the ER; WFS1 directly binds to vesicle cargo proteins (including proinsulin) through the C-terminus of the ER lumen, acts as a transport receptor for vesicle cargo proteins, and its pathogenic mutation located at the C-terminus of the ER lumen hinders the transport of proinsulin to the Golgi apparatus for processing, disrupting insulin secretion and leading to diabetes [9]. The gene discussed is INS; the disease is diabetes mellitus.