Lung adenocarcinomas exhibit various patterns of genomic alterations. During the development of this cancer, serves as a driver oncogene with a relatively high mutational frequency. Emerging data suggest that lung adenocarcinomas with mutations can show enhanced PD-L1 expression and additional somatic mutations, thus linking the prospect of applying immune checkpoint blockade therapy to this disease. However, the responses of -mutant lung adenocarcinomas to this therapy are distinct, which is largely attributed to the heterogeneity in the tumoral immune milieus. Recently, it was revealed that -mutant lung adenocarcinomas simultaneously expressing either a or mutation typically have different immune profiles of their tumours: tumours with a co-mutation generally present with a significant upregulation of PD-L1 expression and tumoricidal T-cell accumulation, and those with a co-mutation are frequently negative for PD-L1 expression and have few tumoricidal immune infiltrates. In this regard, interrogating or mutation in addition to PD-L1 expression will be promising in guiding clinical use of immune checkpoint blockade therapy for -mutant lung adenocarcinomas.