ARL11 (ADP-ribosylation factor-like GTPase 11) is a GTP-binding protein involved in intracellular protein transport and vesicle-mediated trafficking with emerging roles in cancer biology and immune regulation. As a tumor suppressor, ARL11 exhibits pro-apoptotic properties 1, though its canonical functions extend beyond this role. Mechanistically, ARL11 regulates mitogen-activated protein kinase (MAPK) signaling in macrophages, specifically promoting ERK and p38 phosphorylation required for immune cell activation and inflammatory responses 2. In breast cancer, ARL11 interacts with STING to enhance innate immunity and forms positive feedback with type I interferon induction 3. Notably, ARL11 also facilitates DNA homologous recombination repair by interacting with the RUVBL1/2 complex, contributing to PARP inhibitor resistance in breast cancer 3. Disease relevance includes associations with chr13 lymphocytic leukemia and roles in bladder carcinogenesis, where ARL11 silencing dysregulates urothelial differentiation 4. In cutaneous melanoma, ARL11 upregulation correlates with improved patient survival and enhanced immune infiltration, particularly CD8+ T cells and M2 macrophages 5. Clinically, elevated ARL11 expression in breast cancer patients suggests potential therapeutic value; targeting ARL11 alongside RUVBL1/2 may enhance PARP inhibitor sensitivity 3.