In postpubertal females, proapoptotic signaling is central to hormone-dependent endometrial deciduation during menstruation; consistent with this, another hormonally induced human tumor subtype—endometrioid endometrial cancers—exhibits PTEN loss and/or PI3K oversignaling in 90% of cases, often associated with Apert-like FGFR2 mutations [135, 192] that upregulate FGFR2c [193]. Here, PTEN is linked to neoplasm.