This was illustrated by the association of T2D risk with a fine-mapped splice variant that creates a premature stop codon in ERO1B. This newly reported locus is supported by an independent T2D association signal observed in FinnGen, as well as prior experimental and genetic studies that point to a central role in ER homeostasis, insulin biosynthesis, and diabetes progression [53–55]. This evidence concerns the gene INS and type 2 diabetes mellitus.