Alternatively, in this context, the inactivation of tumor suppressors such as phosphatase and tensin homolog deleted on chromosome 10 (PTEN) or depletion of the inositol polyphosphate 4-phosphatase type II (INPP4B) also leads to hyperactivated PI3K/AKT signaling8–10. The gene discussed is AKT1; the disease is neoplasm.