Importantly, there are strong feed forward mechanisms between the factors able to activate STAT3 and what genes STAT3 itself activates, intrinsically in tumor cells themselves as well as in the hematopoietic and stromal compartments, explaining perhaps the constitutive or at least hyperactivation of STAT3 in almost all cancers and highlighting its role as a bona fide oncogene. This evidence concerns the gene STAT3 and neoplasm.