KSHV reactivation from latency is a complicated process which is regulated by an intricate relationship between viral and cellular factors. The method in which resveratrol may regulate KSHV reactivation has yet to be fully understood. However, we propose that resveratrol may inhibit KSHV reactivation by altering the interactions between cellular Egr-1 and viral ORF50P in a Raf.MEK.ERK-dependent manner. All three MAPKs (ERK, p38, and JNK) have been shown to positively regulate Egr-1 expression [41] . However, the role for active p38 MAPK is not fully understood as it has been shown to reduce Egr-1 expression in B-lymphocytes unlike ERK and JNK [42] . Further studies are required to better understand the involvement of different MAPKs on Egr-1 expression during KSHV infection. The findings presented in this study open a Pandora's Box of questions pertaining to treating/managing a variety of viral infections using RDS. Future studies are aimed at appreciating the cellular milieu critical for the effectiveness of the MAPK associated signaling in inducing virus reactivation. These findings may provide for more useful applications to combat a variety of viral lytic infections.