Combined with the results of proteomic and phosphoproteomic data analysis of the anti-PD-1 treatment cohort, we found that the upregulation of MAPK7 (ERK5) kinase activity and NFκB transcription activity may lead to more T cells being recruited into the tumor microenvironment, thereby increasing the sensitivity of patients to immunotherapy. The gene discussed is PDCD1; the disease is neoplasm.