,4 Clinical resistance to immune checkpoint blockade (ICB), such as antibody therapies targeting programmed cell death 1 (PD-1) and CTLA-4, has been associated with somatic mutation and homozygous inactivation of IFN-γ pathway components in tumor cells,5,6,7,8 or inactivation of genes involved in antigen processing and presentation (e.g., B2M)9,10 that are expressed in response to IFN-γ. Here, PDCD1 is linked to neoplasm.