Cytotoxic CD4+ cells may be subject to additional regulatory interactions (beyond the KLRG1/E-cadherin axis) with other suppressive elements of the tumor microenvironment; in addition, N-cadherin, another KLRG1 ligand, becomes upregulated when E-cadherin is downregulated during epithelial-mesenchymal transition, and N-cadherin’s relevance as a functional inhibitory KLRG1 ligand remains to be explored. This evidence concerns the gene CDH2 and neoplasm.