Other experimental approaches involved the use of a cyclin-dependent kinase 7 inhibitor to induce replication stress and genomic instability, which resulted in enhanced response to ICB in mouse lung cancer (47), and in mouse melanoma model, the use of UVB-mutagenized YUMM1.7 cells to generate tumors, resulted in favorable response to ICB treatment (20). This evidence concerns the gene CDK7 and lung cancer.