Unlike cutaneous melanoma, which usually harbors NRAS or BRAF mutations [17], UM is usually initiated by an oncogenic mutation in GNAQ (43%) or GNA11 (49%) [18], which results in constitutive activation of multiple downstream signaling cascades, including the PI3K–AKT, mitogen-activated protein kinase (MAPK), and yes-associated protein 1 (YAP1) pathways [18], thus stimulating abnormal cell proliferation. Here, YAP1 is linked to cutaneous melanoma.