SUGCT and disease arising from reactivation of latent virus: These results suggest that expression of miR‐K12-3 and miR-K12-11 both contribute to the maintenance of latency in endothelial cells, and are consistent with the antagomir inhibition experiments in PEL cells which measured expression of RTA, ORF59, ORF19 and virus production during latent infection (Figure 1).