Leucettinib-92 treatment also improved glucose tolerance, and glucose-induced insulin secretion in vivo.<h4>Conclusions</h4>We show that DYRK1A inhibition restores the β cell mass and function in a preclinical model of T2D, leading to the improvement of body's global glucose homeostasis. The gene discussed is DYRK1A; the disease is type 2 diabetes mellitus.