Furthermore, PDK1 was proven to be required for anchorage-independent growth and xenograft formation of BC cells (MDA-MB-231 and T47 D cells) harboring either PI3 KCA or KRAS mutations attributed to the facts that PDK1 knockdown led to increased anoikis, reduced soft agar growth, and indubitable apoptosis inside tumors, which could be rescued by wild-type PDK1 instead of inactivated mutant PDK1; however, this could not be reverted by constitutively activated AKT in PDK1-silencing cells. Here, AKT1 is linked to breast cancer.