Human cytomegalovirus (HCMV) protein pUL36 was found to bind mixed lineage kinase domain-like protein (MLKL) and target MLKL for degradation in HCMV-infected TERT-immortalized primary human fetal foreskin fibroblasts (HFFF-TERTs) (Fletcher-Etherington A et al. 2020). Furthermore, mutation of pUL36 Cys131 abrogated MLKL degradation and restored necroptosis in HFFF-TERTs. The same residue was also required for pUL36-mediated inhibition of apoptosis by preventing proteolytic activation of procaspase-8, suggesting that pUL36 acts as a multifunctional inhibitor of both apoptotic and necroptotic cell death (Fletcher-Etherington A et al. 2020; Skaletskaya A et al. 2001).