Since the establishment of GNAQ/GNA11 as key oncogenic drivers in a large cohort of UM, genetically engineered overexpression of GNAQQ209L in mice deficient for p16Ink4a and p19Ink4b have been developed which demonstrate elevated YAP signalling downstream of oncogenic GNAQ. However, there was a high incidence of cutaneous melanoma, as opposed to UM in these models. This evidence concerns the gene GNAQ and cutaneous melanoma.