We speculate that a normal Wnt/β-catenin expression maintains the basal expression of TTF-1 expression and a differentiated cell state, whereas activation of Wnt/β-catenin signaling would have an effect on tumour progression (occurs consequently to mutations within the molecular Wnt signaling partners leading to a continuous activation of β-catenin and thus of TTF-1) or tumour regression (through inactivation of GSK-3β by chemical molecules such as LiCl leading to moderate TTF-1 activation). This evidence concerns the gene GSK3B and neoplasm.