Additionally, loss of costimulatory molecules (e.g., CD86, CD54) [14], overproduction of checkpoint inhibitory molecules (e.g., PD-1, CTLA4) [15] and tumor production of the tryptophan degrading-enzyme indoleamine 2,3-dioxygenase (IDO), which eliminates tryptophan, a key amino acid required for T-cell proliferation [16], are other examples of mechanisms utilized by tumors to evade cytotoxic T cells. The gene discussed is ICAM1; the disease is neoplasm.