The ER stress response that is triggered by suppression of fatty acid synthesis may regulate the accumulation of intracellular lipids, since limiting ER stress by deletion of Xbp1, an ER stress response factor (Oakes and Papa, 2015), decreases tumor-derived lipid accumulation in cDCs and enhances their ability to prime CD8 T cells (Cubillos-Ruiz et al., 2015). The gene discussed is CD8A; the disease is neoplasm.