In general, cHL holds the highest reported responses to PD-1 inhibition in any tumor type [82,83], likely because of its genetically driven PD-L1 upregulation, the high mutational burden, the high frequency of MHC-II expression on HRS cells, the CD4+-enriched microenvironment and the abundance of PD-L1+ TAMs. The gene discussed is CD274; the disease is neoplasm.