PLEK (pleckstrin; also known as p47) was originally identified as the major PKC substrate in platelets and later is found to be expressed in all cells of the hemopoietic system. Through two pleckstrin homology (PH) domains at its N and C termini,PLEK may interact with various protein and/or lipid ligands and serve as an intracellular adaptor/targeting protein. Predominantly cytosolic in unstimulated cells,PLEK would undergo transient redistribution to phagosomal membrane in response to stimuli. PLEK has been found to be hyperphosphorylated in diabetic mononuclear phagocytes and promote proinflammatory cytokine secretion in diabetes. (10477609,17579087)