One proposed mechanism for T cell retention in inflamed sites involves upregulation of integrins α1β1 (VLA-1) and αEβ7 (CD103) which are markers of tissue-resident memory T cells and enable adherence of T cells to collagen IV and E-cadherin in peripheral tissues; these have been identified at high frequency in CD8+ T cells infiltrating the VSME (after peptide + IFA vaccines) and in the melanoma tumor microenvironment [46,66,67] and may contribute to both the acquisition of a memory-like phenotype and enhanced lymphocytic trafficking and motility [68]. The gene discussed is CD8A; the disease is neoplasm.