Other well‐studied signalling systems dependent on STAT3 include G‐CSF receptor signalling, HGF and IL‐10.31 Apart from promoting SHh signalling activation, the mechanism by which 44‐mer increases LSC population may also involve the direct binding of STAT3 to the △Np63α promoter.32 Crosstalk between SHh and STAT3 has been studied in gastric metaplasia, lung adenocarcinoma and skin tumours. The gene discussed is HGF; the disease is skin neoplasm.