For instance, pharmacological inhibition of XBP1 or targeting other downstream sensors of ER stress, such as C/EBP homologous protein (CHOP) and protein kinase R-like endoplasmic reticulum kinase (PERK)/endoplasmic reticulum oxidoreductase 1 alpha (ERO1α) have been shown to improve the effector function of tumor-reactive CD8+ T cells.3,4 The insightful work of Hwang et al. adds another exciting piece to the puzzle of overcoming the challenges of ER stress in TME. This evidence concerns the gene ERO1A and neoplasm.