It is speculated that the reason for this may be due to the fact that high HOXB-AS4 expression also upregulates other immune checkpoints such as CTLA4, HAVCR2, LAG3, etc., which may play alternative roles and continue to promote tumor immune escape after PD1 blockade on the one hand, and on the other hand, it is possible that the complex tumor microenvironment containing various immune cells and signaling pathways collectively impact immune inhibitor efficacy. Here, PDCD1 is linked to neoplasm.