The lack of correlation among GNAQ, BAP1, EIF1AX, and SF3B1 proteins and tumor genetic (monosomy and disomy chromosome 3) and clinical characteristics (especially tumor thickness and LBD) may be due to the independence of genetics/proteomics from tumor size, as demonstrated for small UM with the intrinsic ability to metastasize, or to the limited sample size.1 This evidence concerns the gene BAP1 and neoplasm.