However, they lack classical costimulatory molecules such as CD40, CD80, and CD86, which are necessary for the full activation and clonal expansion of CD4+ T cells following T cell receptor (TCR) engagement.[9] Therefore, apCAFs are able to induce naive CD4+ T cells to enter the differentiation pathway of Tregs, further inhibiting the activity of other immune cells, including CD8+ T cells for facilitating tumor evasion of the immune system. The gene discussed is CD80; the disease is neoplasm.