STAT signalling. On binding of IL-6 or IL-11 to the α-subunit of their receptors—which is followed by receptor heterodimerization with the gp130 receptor—JAKs are activated and phosphorylate tyrosine residues in the cytoplasmic region of gp130, which lead to the recruitment of SHP2, STAT3 or STAT1 monomers. These STATs can bind to gp130 through their SH2 domains and become phosphorylated before their dimerization and translocation to the nucleus. Growth factors and non-receptor tyrosine kinases—such as SRC and ABL—can also activate STAT3 signalling. Growth factor receptors that are known to activate STAT3 include the epidermal growth factor receptors EGFR and HER2, vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor (PDGFR), insulin-like growth factor (IGFR), hepatocyte growth factor (HGFR) and fibroblast growth factor receptor (FGFR). ABL, Abelson leukaemia protein; gp130, glycoprotein of 130 kDa; IL, interleukin; JAK, Janus kinase; SRC, sarcoma kinase; STAT, signal transducer and activator of transcription.