Mechanistically, GSK-3 inhibition promoted the upregulation of lymphocyte function associated antigen 1 (LFA-1) in NK cells, and of intercellular adhesion molecule-1 (ICAM-1) on AML target cells, resulting in a stable adhesion of NK cells to their target cells and thereby promoting AML-NK cell conjugates and the subsequent killing of AML cells. The gene discussed is ICAM1; the disease is acute myeloid leukemia.