These scaffolding proteins may participate in ALK-fusion protein-mediated downstream pathway activation; therefore, combinatorial inhibition of the interaction of EML4-ALK and the respective signaling protein(s) by competitive binding peptides or inhibitors as well as by downregulation/degradation of scaffolding proteins might improve therapeutic response of EML4-ALK driven NSCLC patients to ALK inhibitor therapy. The gene discussed is ALK; the disease is non-small cell lung carcinoma.