Previous studies showed that canonical genomic aberrations arise early in UM and give rise to one of three principal evolutionary trajectories associated with signature driver mutations—EIF1AX in class 1 A, SF3B1 and other splicing mutations in class 1B, and BAP1 in class 2 tumors9,10, yet the single-cell resolution of our current findings reveal that these tumors continue to evolve with the development of heretofore unrecognized non-canonical CNV subclones that may contribute to tumor progression, as suggested by recent work13. Here, SF3B1 is linked to neoplasm.