Blocking the binding of Aggrus/podoplanin to CLEC-2-expressing platelets could be a novel therapeutic approach with benefit for EML4-ALK+ patients.[25] ALK has recently been shown to regulate the production of vascular endothelial growth factor A (VEGFA) in anaplastic large-cell lymphoma and EML4-ALK-rearranged NSCLC, and the anti-VEGFA antibody bevacizumab strongly impaired the growth of anaplastic large-cell lymphoma in mouse xenografts [26]. The gene discussed is ALK; the disease is non-small cell lung carcinoma.