STAT3 and neoplasm: Tumour escape may be attributable to tumour genetic changes that affect tumour recognition by immune effective cells (such as, loss of antigen expression, loss of MHC components, shedding of NKG2D ligands and development of IFN-γ insensitivity) or provide tumours with mechanisms to escape immune destruction (such as, defects in death-receptor signalling pathways or expression of antiapoptotic signals including constitutively active STAT3).