The second messenger phosphatidylinositol(3,4,5)tris phosphate is metabolised by both PTEN (a ubiquitously expressed 3’ phosphatase) and SHIP-1 (a 5’ phosphatase restricted to haematopoetic cells). However reactive oxygen species (ROS) inactivate PTEN by causing its catalytic cysteine to form a disulphide bond with a neighbouring cysteine residue. ROS are generated in many signalling pathways and are also produced in some antileukaemic chemotherapies and disease states such as rheumatoid arthritis, where they may influence the survival of T lymphocytes. It has previously been shown that in leukaemic T cell lines that expression of SHIP-1 protects against H2O2-induced cell death and promotes activation of the classical NFκB pro-survival pathway (Gloire et al. 2006). Here we demonstrate that in primary human T cells and the leukaemic T cell line CCRF-CEM, SHIP-1 is phosphorylated and recruited to the cell membrane in response to H2O2. We further show that transfection of the SHIP-1 negative J6 Jurkat leukaemic T cell line with a constitutively active CD2:SHIP chimera protects against cell death in response to ROS. Finally we examine the role of SHIP-1 in apoptosis caused by cytokine deprivation and Fas ligand, both of which utilise ROS-dependent pathways.