T cell-produced IFNγ and TNFα were shown to be critical for bystander killing of antigen loss variants in mouse models [44], and studies showing fibroblast lysis in graft-versus-leukemia models suggested that a local pro-inflammatory environment led to upregulation of adhesion molecules on surrounding tissue and granzyme B-mediated apoptosis of bystander cells when in direct contact with T cells [45]. The gene discussed is GZMB; the disease is leukemia.