A recent study in the zebrafish model showed that hyperactive ERK may be dispensable for UM pathogenesis, and demonstrated that YAP was sufficient to lead to tumor growth and was active when GNAQ, CYSLTR2 and PLCβ4 were mutated, thus suggesting that targeting YAP could be a more promising therapeutic strategy for UM than PKC/MEK/ERK inhibitors [53]. The gene discussed is YAP1; the disease is neoplasm.