Patients with deep-infiltrating endometriosis had lesions with 21% harboring somatic mutations in ARID1A, PIK3CA, KRAS, and PPP2R1A. 9Suda et al., detected activating mutations on KRAS and PI3KCA in 38% and 29% of endometriotic lesions, respectively, with a marked increase in the mutant allele frequency from normal epithelium to endometrial tissue, confirming these cancer-associated mutations as putative selective growth advantages leading to the development of endometriosis and a widespread distribution of the clone across the endometriotic lesions.13 This evidence concerns the gene PPP2R1A and endometriosis.