Given that many CAD antihistamines function that enhance the activity of established cytotoxic or targeted agents, future work should evaluate azelastine in rational combination regimens—for example with taxanes, anthracyclines, platinum compounds, or PARP inhibitors—to determine whether ARF1-dependent mitochondrial and lysosomal stress can be leveraged to lower the effective dose, overcome drug resistance, and achieve more profound tumor control than is possible with azelastine alone [11,12,29,30]. This evidence concerns the gene ARF1 and neoplasm.