Treating human β-cells with polyinosinic-polycytidylic acid (PolyI:C), which mimics viral infections contributing to the development of T1D, resulted in decreased expression of β cell–specific genes such as Ins, MafA, and Slc30A8, along with a marked increase in progenitor markers such as Sox9, Hes1, and Myc (42). The gene discussed is INS; the disease is type 1 diabetes mellitus.