Constitutive activation of STAT3 in NSCLC occurs via several mechanisms: (1) mutated receptor tyrosine kinases (e.g., EGFR) and receptor-independent tyrosine kinases (e.g., SRC), (2) increased cytokine and growth factor levels within the tumor that can activate STAT3, and (3) deregulation of the endogenous STAT3 inhibitors, including PTPs, PIAS, and SOCS [18,19,20,21,22]. Here, STAT3 is linked to neoplasm.