Laffitte and colleagues reported that activation of endogenous NFAT signaling in response to small molecule suppression of Dyrk1a in rat islets [37], yielded transcriptional changes similar to what we report here, including cell cycle regulatory genes (e. g., Ccna1, Aurkb, Cdk1, Dtl, Mki67, and Ccnb2) and T2D GWAS candidates (e. g., Pparg, Kcnk16, Cenpw, Tcf19, Prc1, and Kif11). The gene discussed is KCNK16; the disease is type 2 diabetes mellitus.