However, our results suggest that ERAS does not specifically degrade the mRNA of an unstable protein species, but that multiple ER stress-inducing factors such as cpl-1*, ATM, tunicamycin, thapsigargin, sel-11 LOF and viral infection act on ERAS to mediate ERQC, independent of the protein fold status of the gene product (Figs. 2g–i, 3c,d, 4g–m and 5 and Extended Data Fig. 3). The gene discussed is ATM; the disease is viral infectious disease.