Altogether, these findings showed that increased Gal-3 protein expression in the hBM-MSCs-conditioned AML cell line decreased β-catenin degradation by stimulating AKT and GSK-3β phosphorylation, leading to the enhanced transcription of β-catenin target genes, such as cyclin D1 and c-myc, hence promoting AML cell drug resistance. The gene discussed is MYC; the disease is acute myeloid leukemia.