While inhibitors of the cell cycle regulator dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) have been successfully combined with TGF-β inhibitors or glucagon-like peptide-1 (GLP1) analogues to promote human beta cell transdifferentiation from alpha cells, further enhancing in vivo beta cell numbers with additional drugs may be necessary for clinical effect in established type 1 diabetes [53] (Fig. 2d). Here, DYRK1A is linked to type 1 diabetes mellitus.