Efficient clearance of apoptotic cells through efferocytosis is essential for maintaining stability in metazoans. Macrophages are key players in innate immunity during this process, releasing anti-inflammatory cytokines such as IL-10 and TGF-beta to create an immunologically quiet environment. While normal efferocytosis supports tissue tolerance and reduces inflammation, tumors often exhibit high levels of apoptosis, resulting in excessive efferocytosis and an immunosuppressive environment. This condition allows tumors to evade immune responses, diminishes CD8+ T cell activity, and promotes tumor growth. Our previous research identified Mertk, a TAM receptor tyrosine kinase (Tyro3, Axl, Mertk), as a critical inhibitory receptor that boosts macrophage efferocytosis and immune suppression, facilitating tumor development. Blocking Mertk, either genetically or with drugs, can restore immune function and enhance anti-tumor responses. In this study, we investigated a CR-Mertk transgenic mouse with a mutant form resistant to ADAM17 cleavage, inserted into the native Mertk gene. Results show that CR-Mertk acts as a gain-of-function mutation, increasing Mertk expression on cell surfaces, promoting efferocytosis, and raising TGF-beta levels. In an orthotopic EO771 Triple Negative Breast Cancer model, CR-Mertk mice exhibited increased tumor fibrosis and lung metastasis compared to wild-type mice. Ongoing work includes analyzing the effects of the efferocytosis secretome on fibroblasts and conducting bulk RNA sequencing to compare metabolic pathways, pro-resolution genes, and other M2 polarization markers between wild-type and CR macrophages during efferocytosis.