This is of particular relevance, given that Gαq/11 mutations enhanced susceptibility to YAP-TEAD inhibition via treatment with the YAP-TEAD inhibitor verteporfin in vitro [178], suggesting that cancers driven by these G protein subfamilies, as well as GPCRs that regulate them, may be vulnerable to therapeutic targeting of Hippo pathway effectors. Here, GNAQ is linked to cancer.