The role of both isoforms is less well studied in CRC and the picture is less clear-cut and dependent on the model system used; AKT2 seems to be similarly important for metastasis formation by CRC cell lines [65,66,67] and a recent study using genetically engineered mouse models reported that combining TP53 inactivation with expression of constitutively active AKT1E17K and azoxymethane treatment gives rise to aggressive, metastatic tumours resembling the mesenchymal CMS4 subtype [68]. The gene discussed is TP53; the disease is neoplasm.