In breast cancer, overexpression of FXYD5 was associated to increased activation of AKT.38 The inhibition of AKT suppressed FXYD5’s ability to activate NF-kB pathway and to promote cell mobility and tumour cell invasion.38 Further studies are necessary to identify pathways involving FXYD5, and tumours that could benefit of an FXYD5-targeted therapy, as suggested by a recent research reporting the efficacy of a novel antibody-drug conjugate for the selective growth inhibition of thyroid cancer cells expressing moderate to high dysadherin on cell surface.51 This evidence concerns the gene AKT1 and thyroid gland carcinoma.