Furthermore, since the interaction between ILT7 and BST2 needed to be stabilized with cross-linking agents in cellulo (Fig 8C, 8D and 8E) and that close cell-to-cell contact was required to achieve activation of ILT7 by BST2-expressing transformed or cancer cells [25], it remains to be demonstrated whether contacts between activated pDCs and bystander normal T cells (as opposed to transformed or infected cells) would be frequent and sustained enough to engage the BST2/ILT7 negative feedback system. The gene discussed is BST2; the disease is cancer.