Glycosylation site deletions increase the ability of NA from A/Puerto Rico/8/1934 (H1N1) to induce ER stress . Deletion of the N219 glycosylation site from NA of another H1N1 virus, A/WSN/1933, similarly increases UPR markers and retention of NA within the ER . Whether UPR activation is a desirable or undesirable outcome that may contribute to a tendency for IAV viral glycoproteins to acquire glycosylation mutations remains to be determined.