Long-standing or suboptimal treatment of achalasia may cause stasis and slow elimination of foods, bacterial overgrowth, and prolonged acid exposure to the esophageal mucosa with reflux symptoms.2 This creates an environment prone to chronic inflammation and damage to the esophageal mucosa, ultimately increasing the risk for hyperplastic changes and malignant transformation with time.5–7 Studies have also suggested increased frequency of p53 overexpression in patients with achalasia, potentially increasing the risk of ESCC.8,9. This evidence concerns the gene TP53 and esophageal squamous cell carcinoma.