Irrespective of the high density of T lymphocytes in tumor infiltrate, T cell exhaustion controlled by elevated expression of B7-H1, PD-1, CTLA4, CD160, LAG-3, Tim-3+ and T cell aging mediated by upregulation of CD57, KLRG-1, and Tim-3 was found to play a crucial role in triggering HCC recurrence after curative treatments [85]. The gene discussed is CD274; the disease is neoplasm.