The proinflammatory effects and endoplasmic reticulum stress (ERS) induced by the HLA-B*35 allele, combined with the Th2-promoting capability of DRB1*11, may explain the increased incidence of immune-related pneumonitis (IRP) in cancer patients receiving PD-1/PD-L1 immune checkpoint inhibitor therapy (42, 44). The gene discussed is CD274; the disease is cancer.