Persistent activation of STAT3 in cancer cells is attributable to autocrine or paracrine cytokine stimulation in the tumor microenvironment, expression of various oncogenic protein tyrosine kinases (e.g., Src) or oncogenic fusion proteins (e.g., nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)), and mutation of STAT3 pathways [110,111,112,113]. Here, NPM1 is linked to neoplasm.