Additionally, knockdown of KAP1 in KSHV-infected primary effusion lymphoma (PEL) cells reduced viral episome stability and enhanced the efficiency of KSHV lytic reactivation by hypoxia, suggesting that both KAP1 and the cooperative interaction of RBS HRE within the RTA promoter are crucial for KSHV latency and hypoxia-induced lytic reactivation [63]. Here, TRIM28 is linked to primary effusion lymphoma.