Research using neuronal models of CCH has demonstrated that zinc-induced neurotoxicity plays a role in its pathogenesis, leading to the upregulation of ER stress-related genes, such as CCAAT-enhancer-binding protein homologous protein (CHOP) and growth-arrest- and DNA-damage-inducible gene 34 (GADD34) [53]. The gene discussed is DDIT3; the disease is columnar cell hyperplasia of the breast.