Parallel research by the Xiao et al. team proved that: 1) in vivo, Pdx1, and MafA expression reprograms mouse α cells into β cells, 2) normalization of β-cell toxin-induced diabetic mice was achieved using reprogrammed β cells, 3) delayed onset diabetes was seen in autoimmune NOD mice due to reprogrammed β cells, and finally, 4) in vitro, Pdx1, and MafA expression reprogrammed human α cells into β cells. This evidence concerns the gene PDX1 and diabetes mellitus.