However, a large scale screen for gene inactivations that render cells more sensitive to proteasome inhibitors supports a model that human DDI1 protease also processes Nrf1: DDI2 (one of two human orthologues of DDI-1) and Nrf1 were highly ranked hits in this screen that identified hundreds of gene inactivations that increase sensitivity of multiple myeloma cells to proteasome inhibitors (Acosta-Alvear et al., 2015). The gene discussed is DDI2; the disease is AL amyloidosis.