AKT1 and neoplasm: On the other hand, Bozzi et al. suggested that the overexpression of several tyrosine kinase receptors that signal through AKT contributes to the proliferation of these tumor cells through β-catenin stabilization [23], since mutations in APC (Adenomatous Polyposis Coli) or β-catenin, which would promote its nuclear accumulation, are rare in synovial sarcoma [34, 35].