Since the gp130Y757F germline mutation also impairs expression of the stomach-specific tumour suppressor gene tff1 [30], and since all colonic tumours in CAC-challenged gp130Y757F mice harbour mutagen-induced oncogenic conversions of β-catenin, excessive activation of endogenous Stat3 may only promote tumour growth in conjunction with preexisting tumour-initiating mutation(s). Here, STAT3 is linked to colonic neoplasm.