Therefore, it follows that drugs disrupting this complex interaction may be efficacious in counteracting such signal diversification and thereby more effective in combating both primary and secondary resistance in tumours with the appropriate molecular targets.18 In conclusion, we have shown a specific relationship between EGFR and Axl RTKs, enabled through a direct protein-protein interaction, which diversifies the signalling pathways available to EGFR. This evidence concerns the gene EGFR and neoplasm.