NCAM1/CD56 supports chemotherapy resistance and leukemia cell function in AML. The expression of the membrane surface protein NCAM1 or CD56 (NCAM1/CD56) is elevated in approximately 15% to 20% of AML cases. NCAM1 transcription is regulated by a series of transcription factors such as MEIS1, MEF2C, or STAT1. Once expressed and activated on the surface of AML cells, NCAM1 activates the MAPK (MAP-kinase) signaling cascade to promote cell survival and proliferation, resistance to conventional AML chemotherapies, and leukemia stem cell function.