Conversely, in xeroderma pigmentosum (XP), an extremely high mutational burden and neoantigen load theoretically enhance tumour immunogenicity [61]; however, chronic UV-induced inflammation and PD-L1 upregulation may counterbalance this effect, leading to heterogeneous responses to immune checkpoint inhibition [62,63,64]. Here, CD274 is linked to xeroderma pigmentosum.