Immunoblotting analysis supported this finding, showing that IDH1 mutation activated the PERK/ATF4 arm of the UPR in U87 glioma cells (Figure 7C), in keeping with our previous report that PERK/ATF4 signals are central ERS sensors that predispose IDHmt cells to apoptosis.[32] Remarkably, ISRIB, a potent and selective inhibitor of PERK signaling, blocked miR‐19a expression in IDHmt glioma cells in a dose‐dependent manner (Figure 7D), indicating a regulatory role of the PERK/ATF4 arm in miR‐19a expression. The gene discussed is ATF4; the disease is glioma.