In tumor cells, the association of Src with abnormal receptor tyrosine kinases increases the tyrosine kinase activity of Src, thereby activating pro-survival pathways through PI3K/AKT, the angiogenic pathway through signal transducer and activator of transcription 3 (STAT3), the proliferation pathway through MEK/ERK, and invasion through FAK/paxillin/p130CAS [13]. The gene discussed is SRC; the disease is neoplasm.