Moreover, CpdA-03 is less likely to induce therapeutic resistance, as it did not activate FKBP51, the direct GR target gene [48], which is involved in the feedback control of GR signaling via GR retention in the cytoplasm and associated with GC resistance in patients with brain and prostate cancer, melanomas, and lymphomas [49,50]. The gene discussed is NR3C1; the disease is lymphoma.