This suggests that our small molecules could similarly phenocopy the ATF6-dependent reductions in the trafficking and intracellular aggregation of destabilized, aggregation-prone proteins associated with other gain-of-toxicity protein misfolding diseases (e.g., A1AT-Z aggregation in liver disease and rhodopsin aggregation in retinal degeneration (Chiang et al., 2012; Smith et al., 2011)). This evidence concerns the gene ATF6 and proteostasis deficiencies.