In chronic myeloid leukemia (CML), GA reverses resistance to imatinib and doxorubicin by inhibiting BCR-ABL and its downstream STAT5, ERK1/2, and Akt signaling pathways, while reducing pregnane X receptor (PXR) expression (Wang et al., 2020). The gene discussed is NR1I2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.