Much remains to be done to evaluate whether p190A mutations promote malignant transformation of endometrial cancer cells through pathways other than the RhoA-YAP axis, given that RhoA-independent functions of p190A have been reported.25,26 It will also be useful to generate mouse models of conditional endometrial-specific p190A KO to further investigate p190A-null phenotypes in vivo and determine whether the Hippo-YAP pathway is indispensable for p190A mutation-induced endometrial cancer. This evidence concerns the gene ARHGAP35 and endometrial cancer.