Furthermore, it is currently unclear why EBNA3A plays only a subsidiary role in the regulation of ADAM28 and ADAMDEC1 compared to EBNA3C, or why EBNA3A is found on the COBLL1 peak (S4 Fig) even though in the primary B cell infection the presence of EBNA3A is clearly not required in the repression of COBLL1. This is unlikely to be an artefact of our TAP-tagged LCL cell lines, because two recently published ChIP-seq experiments using anti-HA antibody in EBNA3A-HA [68] or EBNA3C-HA [67] LCL obtained similar results and detected both EBNA3A and EBNA3C at ADAM and COBLL1 peaks (S8A and S9A Figs). Here, ADAMDEC1 is linked to infection.