The mechanisms underlying aberrant STAT3 activation during tumor development include autocrine action of cytokines, cytokine receptor amplification and activating mutations, gain-of-function mutations in STAT3 and JAKs, and loss of function mutations in negative regulators (e.g., Protein Tyrosine Phosphatase Receptor Type T (PTPRT), SOCS1, and SOCS3), depending on the types an the stages of individual cancers [5,6,9,10,11]. This evidence concerns the gene STAT3 and neoplasm.