The primary tumor arises through an initiating mutation in one of several genes in the Gaq/11 signaling pathway (GNAQ, GNA11, PLCB4, or CYSLTR2), followed by a “BSE” progression mutation in BAP1, SF3B1 (and rarely other splicing factors), or EIF1AX, associated with high, intermediate, and low metastatic risk, respectively1–7. Here, BAP1 is linked to neoplasm.