It has been previously demonstrated that adhesion of multiple myeloma cell lines can inhibit specific anticancer immune effectors, specifically the death receptor CD95/Fas/Apo-1. This protection involves the intracellular redistribution of cellular FLIP, a survival protein. This grant proposes to identify the specific mechanism(s) by which adhesion mediates the redistribution of FLIP (and increased survival). These findings may aid in the development of pharmacological agents that assist the human immune system to eliminate multiple myeloma cells.