Epidermal growth factor receptor （EGFR）-mutant advanced non-small cell lung cancer （NSCLC） was previously regarded as a cold tumor according to tumor immune microenvironment （TIME）. However，recent studies have found that EGFR-tyrosine kinase inhibitors （EGFR-TKIs） treatment can transform the host immunity from immunosuppressive to immunosupportive state，bringing new hope for immunotherapy. There are four main therapeutic strategies for patients after EGFR-TKIs acquired resistance： immunotherapy alone （Im），immunotherapy plus chemotherapy （Im+C），immunotherapy plus antiangiogenic drugs （Im+A），and immunotherapy combined with antiangiogenic drugs and chemotherapy （Im+A+C）. Among them，the efficacy of Im is extremely limited，being significantly lower than that of chemotherapy alone，while there is still scarce evidence for the efficacy of Im+A with few clinical studies. The combination of Im+C and Im+A+C shows better efficacy than chemotherapy alone. Im+A+C has a superior clinical outcome to Im+C. Additionally，the EGFR L858R mutation subgroup benefits more from Im+C than the EGFR 19 del mutation subgroup. The T790M-negative subgroup has a greater benefit from Im+A+C than the T790M-positive subgroup. In general，the strategy of combining immunotherapy with chemotherapy and/or an antiangiogenic drug represents a novel and promising method for treating EGFR-mutant NSCLC after EGFR-TKI failure.