Previous large-scale sequencing studies of endometrial cancer detected an unexpectedly high frequency of loss-of-function mutations in p190A.7,8 RhoA GTPase was previously reported as a positive upstream regulator of YAP activity via its inhibition of LATS1/2 kinases.16 In our study, we revealed that YAP activation represents an important molecular event contributing to p190A inactivation-induced endometrial carcinogenesis, which is dependent on the aberrant activation of RhoA GTPases (Supplementary Fig. 8). This evidence concerns the gene LATS1 and endometrial cancer.