We found a strong correlation between increased NEP transcription and its protein overexpression, suggesting that the protein accumulation is secondary to increased production (as is the case with other oncogenes such as epidermal growth factor receptor and cyclin D1 in lung and esophageal cancer, respectively) rather than an increase in protein half-life or decrease in protein degradation [25-27]. The gene discussed is MME; the disease is esophageal cancer.