EGFR and cancer: These events cause allosteric activation of EGFR kinase and trans-autophosphorylation of tyrosine residues in the cytoplasmic receptor tail, thereby triggering a signaling cascade.[34] In several human cancers, EGFR signaling is abnormally altered by gene amplification and/or protein overexpression, mutation, or in-frame deletion.[35] Somatic EGFR activating mutations have been observed in approximately 15% to 20% of NSCLC patients.[36] Upregulated levels of EGFR have been detected in the mitochondria in NSCLC cells.