The results from denatured immunoprecipitation (IP) assays showed that HNRNPU was dramatically SUMOylated by SUMO1 and SUMO2/3 in iSLK cells with KSHV latent infection (iSLK.219) under normoxic conditions, while the SUMO2/3- but not the SUMO1-modified form of HNRNPU was inhibited by hypoxia (Fig. 7A), indicating that SUMO2/3-modified HNRNPU induced by KSHV infection is involved in the response to hypoxia. The gene discussed is SUMO2; the disease is disease arising from reactivation of latent virus.