Although a larger study is needed to confirm these findings, they align with preclinical studies showing that a loss of PTEN in breast tumor cells is sufficient to drive CDKi resistance.51,59 Upregulation of AKT activity stemming from PTEN loss promotes resistance to both CDKi and PI3Kα inhibitors, which is reversed by treatment with an AKT inhibitor (AKTi). The gene discussed is AKT1; the disease is breast neoplasm.