In CML, GC-induced GILZ expression abolished resistance to tyrosine kinase inhibitors, a drug family used in this syndrome, by inactivating the mammalian target of rapamycin complex-2/AKT signaling pathway and by activating FOXO3A-mediated transcription of the proapoptotic protein Bim, which plays a critical role in cell death induced by tyrosine kinase inhibitors100. The gene discussed is TSC22D3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.