EGFR and brain neoplasm: For example, activation of kinase and cytokine receptor signaling can be achieved by formation of chimeric transcripts merging exons of two partner genes (e.g., BCR-ABL in leukemia [1]), internal tandem duplication (ITD) in the juxtamembrane domain or kinase domain (e.g., FLT3 ITD in leukemia [2], FGFR1 ITD in brain tumors [3]), C-terminal truncation (e.g., EGFR in brain tumors [4] and MAP3K8 in melanoma [5]), promoter swapping (e.g., P2RY8-CRLF2 in leukemia [6]), or enhancer hijacking (e.g., IGH-EPOR in leukemia [7]).