CD8A and neoplasm: Moreover, growing evidence suggests that the tumor resistance to PD1 blockade immunotherapy is probably due to lack of CD8+ T cell infiltration into tumor microenvironment after treatment.[34] The response rate of HNSCC to PD1 blockade is around 20–30%, and the majority of HNSCC were irresponsive to PD1 blockade,[4] suggesting that HNSCC might have an intrinsic mechanism against immunotherapy.