Zeng and colleagues used an isogenic hESC platform to investigate GWAS-identified T2D susceptibility loci, including CDKAL1. Differentiation of CDKAL1 deficient hESCs toward SC-β was not altered, but SC-β showed impaired glucose-stimulated insulin secretion (GSIS), although KCl or arginine-induced secretion was not impacted [208]. This evidence concerns the gene CDKAL1 and type 2 diabetes mellitus.