This mechanism has two key features: first, fibroblasts sample, process and cross-present antigen complexed with MHC I. Second, co-incident antigen-specific upregulation of FAS/FASL and PD-1/PD-L2 on T cells and CAFs respectively, drives the death and dysfunction of tumour specific T cells resulting in enhanced tumour viability. The gene discussed is FAS; the disease is neoplasm.