Resistance to antiangiogenic therapies in cancer involves both tumor cells and stromal components, but their relative contributions differ in each cancer subtype. In this issue of the JCI, Cascone et al. describe a stromal adaptation to antiangiogenic therapy in non–small cell lung carcinoma (NSCLC) models that include EGFR-driven vascular remodeling promoting resistance to VEGF inhibition. Their results suggest that the added benefit of dual VEGF/R and EGFR targeting in these models could be clinically relevant to fight resistance in NSCLC patients.
