They include: (a) impairment of intratumoral Treg expression of FoxP3, resulting in a loss of Treg cell lineage stability and abrogation of intratumoral Treg suppressive function [15], (b) downregulation of exhaustion markers for CD8+ intratumoral T cells increasing their CTL function [16] and (c) generation of high-avidity CTL responses to tumor-associated antigens [17]. Here, CD8A is linked to neoplasm.