The expression of ligands to immune checkpoint receptors like CTLA-4 (CD80, CD86) or PD-1 (PD-L1, PD-L2) on the tumor cell surface mediates inhibition of T-cell responses, representing one way of immune evasion that can be pharmaceutically targeted.3 Despite the successful use of present immune checkpoint inhibitors in several cancer entities, many cancer types do not respond to such compounds, suggesting distinct mechanisms of immune evasion that still need to be elucidated. This evidence concerns the gene PDCD1 and neoplasm.