In this model, CD103 expression promotes accumulation of donor CD8 T cells in host tissues via interaction with E-cadherin, which is highly and specifically expressed by cells comprising host epithelial compartments [14] Our data indicate that CD8 T cells unable to express CD103 remain capable of exerting anti-tumor effects – likely through LFA-1-dependent mechanisms[10] - hence providing a mechanistic basis for the separation of GVHD and GVT effects by CD103 disruption. The gene discussed is CD8A; the disease is graft versus host disease.