We found several compounds, known to target p38 MAPK, to inhibit KSHV reactivation after baculovirus RTA and Na-butyrate treatment (figure S1A), in line with previous reports on a role of p38 during de novo infection [88], after induction of productive reactivation [43], and during progression of KSHV through the lytic cycle, when, for instance, vGPCR activates p38 [89]. The gene discussed is MAPK14; the disease is infection.