More recently, a study looking at the peripheral blood mononuclear cells of patients living with sporadic ALS found a significant upregulation of spliced XBP1, and of the two stress sensors IRE1α and ATF6, compared to healthy controls, indicating that UPR induction is not a terminal or near-terminal event but rather a compensatory mechanism, that begins to happen early in the course of the disease [14]. This evidence concerns the gene ERN1 and amyotrophic lateral sclerosis.