To determine whether Gcg+/SstLow cells were a consequence of senescent β cell accumulation during T1D development in NOD mice, we carried out immunohistochemistry for Gcg and Sst on pancreas sections from a cohort of 14-week old NOD mice that had been treated with a senolytic agent ABT-199 (n = 4 mice) or vehicle (n = 5 mice) from 12 until 14 weeks of age (Figure 3). The gene discussed is SST; the disease is type 1 diabetes mellitus.