Molecular profiling in a subgroup of 67 patients in this study confirmed that mutations in PIK3CA and PTEN were more common in endometrioid than non-endometrioid tumors, but were not associated with improved PFS with paclitaxel + sapanisertib compared with paclitaxel in patients with endometrioid histology; however, mutations in the beta-catenin signaling pathway were associated with improved PFS with paclitaxel + sapanisertib compared with paclitaxel in patients with endometrioid histology. Here, PIK3CA is linked to endometrioid tumor.