Senescent cells in lung tumors actively reshape immune responses through their senescence-associated secretory phenotype (SASP), creating a complex microenvironment that can either support or hinder cancer progression. These permanently growth-arrested cells influence antigen presentation and immune cell recruitment while potentially driving adaptive resistance to checkpoint inhibitors in non-small cell lung cancer patients. The emerging therapeutic paradigm of "induce, then edit or eliminate" represents a sophisticated approach to cancer treatment that could significantly improve outcomes. Rather than simply trying to eliminate senescent cells, this strategy first induces senescence in cancer cells to halt proliferation, then selectively clears harmful senescent cells while preserving beneficial immune responses. Senolytics that eliminate senescent cells and senomorphics that reprogram their secretory profiles offer complementary tools for this approach. This framework addresses a critical gap in current immunotherapy, where checkpoint inhibitors show promise but often face resistance mechanisms. The concept is particularly compelling because it leverages the dual nature of senescence—beneficial for stopping cancer growth but potentially harmful through chronic inflammation. Success will depend on precise timing and patient selection based on senescence biomarkers.