The major explanation so far is that the TME is largely heterogeneous and that PC is not a hypermutated disease as other urological cancers16 and that absence of successfully treatment modalities as blocking the axis of PD-1/PD-L1 and CTLA-4/CD80 expression is due to several alterations in these ICP molecules9,12,13. This evidence concerns the gene CD274 and pachyonychia congenita.