Additionally, based on the data from T47D breast cancer cells, it seems that this mechanism might also occur in other PIK3CA-mutant cancer types as well as cervical cancer with PIK3CA mutations, suggesting that the subcellular localization of FOXO3a upon treatment of PI3K inhibitor might become a biomarker predicting the response to the combination therapy with inhibitors of PI3K and autophagy in PIK3CA-mutant cancers. This evidence concerns the gene FOXO3 and breast carcinoma.