Chui MH, et al. - Researchers examined whether endosalpingiosis harbored the driver mutations in BRAF and KRAS which characterize ovarian low-grade serous neoplasms, using laser-capture microdissection and digital droplet PCR. In 14 of 43 endosalpingiotic lesions examined, somatic mutations were identified. Of 21 women with endosalpingiosis correlated with a synchronous or metachronous ovarian low-grade serous tumor, mutations were recognized in endosalpingiotic lesions from 11 women, with most cases (10/11) exhibiting identical mutations in both tumor and endosalpingiosis. On the contrary, only one of 13 cases of endosalpingiosis not related to an ovarian tumor harbored a KRAS mutation. In endosalpingiosis vs low-grade serous tumors, the proliferative activity as evaluated by Ki-67 immunohistochemistry was lower, and endosalpingiosis with either BRAF or KRAS-mutation had significantly lower Ki-67 index in comparison with those without. Ectopic expression of KRAS^G12V in fallopian tube epithelial cells resulted in ERK phosphorylation, p21 induction, growth arrest, and cellular senescence. In conclusion, it was illustrated that endosalpingiosis signifies an impressive example of cancer driver mutations in deceptively normal-appearing cells, which could be inclined to neoplastic changes upon bypass of endogenous oncosuppressive mechanisms.