We used a human CML cell line, K562/ADR cells, as the MDR cell model, and found the following four results: (1) expression levels of GnT-III and its product that bisects GlcNAc were suppressed in the K562/ADR cells; (2) the suppression of GnT-III induced autotrimerization of TNFR2 and NF-κB signaling for the upregulation of P-gp expression; (3) the overexpression of GnT-III in K562/ADR cells rescued these phenomena, as observed in the parental K562 cells; and (4) the deficiency of TNFR2 decreased P-gp expression, but it increased GnT-III expression (Fig. 9). This evidence concerns the gene NFKB1 and chronic myelogenous leukemia, BCR-ABL1 positive.