Prior to these T2D GWAS linkages, our group demonstrated that Cdk4 deficiency led to hypoplasia of insulin-producing pancreatic islet β cells (β cells), whereas expression of constitutively active Cdk4R24C kinase led to early commitment to the β cell lineage (29–31), β cell hyperplasia, and enhanced β cell regeneration (32). The gene discussed is INS; the disease is type 2 diabetes mellitus.