Furthermore, we found that treatment of db/db mice with adipsin, which preserves β-cell mass in diabetic db/db mice23, decreased ChREBPβ abundance in a manner proportionate to the improved glycemia and plasma insulin levels, concordant with the idea that ChREBPβ expression contributes to the glucose toxicity seen in the db/db mouse model of T2D (Fig. 3c–f). The gene discussed is INS; the disease is type 2 diabetes mellitus.