In particular, recently presented results from the phase Ib-II Faktion trial suggested that the activation of the PI3K/Akt/PTEN pathway (defined as activating PIK3CA mutations in tumor tissue/blood or PTEN null by immunohistochemistry in primary or metastatic tumor tissue) did not affect sensitivity to Capivasertib, since a beneficial effect from the addition of the Akt inhibitor to Fulvestrant in HR+ metastatic BC was observed in both PI3K/Akt/PTEN activated and non-activated tumors [40]. The gene discussed is AKT1; the disease is neoplasm.