Effector that acts as an elicitor that induces cell death and promotes ROS accumulation in Nicotian benthamiana (PubMed:27242731, PubMed:28410577). RxLR16-triggered cell death is dependent on SGT1, HSP90 and RAR1, but independent of the somatic embryogenesis receptor-like kinase SERK3/BAK1, indicating that it acts independently of the detection of cell surface pattern recognition receptors (PubMed:28410577). Enhances the expressional levels of defense-associated genes involved in the salicylic acid-, jasmonate acid-, and ethylene-mediated signal transduction, resulting in disease resistance (PubMed:28410577). However, as some other Plasmopara viticola RxLR effectors including RxLR1, RxLR10, RxLR30 and RxLR25, can suppress defense responses and disease resistance induced by RxLR16, it may not trigger host cell death or immune responses during physiological infection under natural conditions (PubMed:28410577). Host nuclear localization is required to elicit cell death. Expression is up-regulated at the earlier infection stages. The RxLR-dEER motif acts to carry the protein into the host cell cytoplasm through binding to cell surface phosphatidylinositol-3-phosphate. N-glycosylated (Probable). The putative N-glycosylation site at position 240 is essential for cell death-inducing activity (PubMed:28410577). Belongs to the RxLR effector family.