In PDAC, CD8+ T-cell activity is altered due to degradation via MHC-1, member of the histocompatibility complex, [150], while inhibition of autophagy restores surface levels of MHC-1, enhancing anti-tumor T-cell response, improving [151] clinical outcomes, increasing the survival rate for PDAC patients [152]; the effect observed in CD4+ T cells depends on their subtype differentiation [153]. Here, CD8A is linked to neoplasm.