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ERS is obviously an adaptive mechanism, which most likely developed for sensing microbes, and which becomes maladaptive when chronically stimulated by overconsumption of carbohydrates and saturated fats; the sequel UPR is notably appropriate for response to microbes, and notably harmful when activated by habitual dietary excess. When ERS-UPR activation is sustained, the result is excess inflammation and immune system hypervigilance (e.g., pathophysiologic priming for disorders of metabolic/allergic/autoimmune inflammation); more intense activation of ERS may result in apoptosis.