Additionally, recent data showed that continued AKT-targeted therapies in luminal BC cells elicited dephosphorylation and nuclear translocation of FOXO3a, and impaired the link between FOXO3a and SirT6, ultimately leading to acetylated FOXO3a, which recognized the BD2 domain of BRD4, recruited the BRD4/RNAPII complex to the CDK6 gene promoter, and induced its transcription. The gene discussed is AKT1; the disease is breast cancer.