Secretion of IFNγ by antigen-specific CD8 T cells in a similar co-culture system demonstrated activation of IFNγ-dependent STAT1 in bystander cells but formation of an immunological synapse was crucial to the release of IFNγ, indicating antigen-specificity of IFNγ release.39 This finding is consistent with our data that activated CD8 T cells do not kill KC unless they express cognate antigen, and that KC deficient in IFNγ receptor are more resistant to cell-mediated cytolysis. The gene discussed is STAT1; the disease is keratoconus.