Nevertheless, the data presented in our study showed that PTEN wild-type cell lines and tumor xenografts resistant to CDK4/6i and fulvestrant (MPF-R and TPF-R cells) benefited from AKT inhibition, demonstrating the need for clinical trials of AKTi in combination with standard CDK4/6i and endocrine therapy in the post CDK4/6i-setting independent of the tumor PTEN status. Here, CDK4 is linked to neoplasm.