The loss-of-function mutation of PTEN includes frameshift mutation and truncated mutation or homozygous deletion, which causes the loss of its functions, i.e., tumor suppression and the hyperactivation of AKT, which furthers lead to cell proliferation, resistance to apoptosis, and the switching of p27 from tumor suppressor to an oncogene [84,85]. The gene discussed is AKT1; the disease is neoplasm.