Numerous pre-clinical studies have highlighted the mechanisms by which this interaction may occur: via the triggering of tumor antigen release, also via an increase in their cross-presentation, an increase in the expression of MHC Class 1 on the plasma membrane (making irradiated cells more recognizable by the immune system), the increased release of pro-inflammatory cytokines and DAMPs, stimulation of the recruitment of cytotoxic CD8+ T lymphocytes in the irradiated lesion’s microenvironment via dendritic cells, and increased cell expression of FAS [25]. This evidence concerns the gene CD8A and neoplasm.