A recent review of low-grade endometrial cancer molecular profiles showed that certain molecular subtypes of (i) POLE-ultramutated tumors; (ii) p53 wild type/NSMP tumors with wild type CCND1 and CTNNB1, are estrogen receptor (ER) and progesterone receptor (PR) positive and lack 1q32.1 amplification, and with low L1CAM expression and DNA damage; and (iii) MMR-deficient tumors with wild type CCND1 are estrogen receptor and progesterone receptor positive, lack PTEN methylation, and, without Lynch syndrome, could be potentially considered low-risk endometrial cancer tumors [67]. This evidence concerns the gene PTEN and endometrial cancer.