Moreover, Cnot3βKO mice displayed a post-transcriptional defect in insulin biosynthesis where Cnot3βKO islets displayed significantly decreased expression of mRNAs encoding proteins involved in insulin biosynthesis, such as T2D-associated zinc transporter Slc30a8, proinsulin-to-insulin convertase (Pcsk2), and carboxypeptidase (Cpe)34,35 (Fig. 4d and Table 1). This evidence concerns the gene INS and type 2 diabetes mellitus.