Consistent with this, we have recently demonstrated that loss-of-function PTEN mutations (PTEN C124S/+ and PTEN G129E/+) coupled with oncogenic PI3K (PIK3CA H1047R) lead to AKT hyper-activation in a mouse model of breast cancer and that, although resistant to alpelisib, PTEN and PI3K mammary organoids are sensitive to the AKT inhibitor MK-2206 [139]. The gene discussed is AKT1; the disease is breast carcinoma.