Ever since the description of  tumors occurring during long-term profound acid inhibition by either proton pump inhibitors (PPIs)  or the insurmountable histamine-2 antagonist loxtidine  there has been concern about cancer risk also in patients being treated long-term with PPIs. The neoplasia secondary to profound acid inhibition was soon recognized to be due to hypergastrinemia secondary to gastric hypoacidity . Also, in patients, the initial step in the neoplasia development in rodents , hyperplasia of the target cell of gastrin, the ECL cell, was  described , and ECL cell derived gastric  neoplasia of different degree of malignancy had been known in man before the introduction of PPIs. Nevertheless, the  medical society accepted that PPIs posed no risk of cancer in man . With time some reports describing ECL carcinoids secondary to PPI treatment appeared ), and we have repeatedly described that the ECL cell probably was the cell of origin of many gastric carcinomas . Nevertheless, the general view was that PPI treatment was without any risk of gastric neoplasia until Cheung et al. described increased risk of gastric cancer in patients taking PPI after Helicobacter pylori eradication . Despite confirmation by others  this finding has been met with skepticism . Moreover, and curiously, the study by Cheung et al. (15) has not been commented on by American journals. Now, in “Gastroenterology”, a large follow up study of patients treated with pantoprazole for on average 3 years did not show any indication of neoplasia in the gastrointestinal tract, and the journal published an “Editorial” with the title: Safety and complications of long-term proton pump inhibitor therapy: Getting closer to the truth. The “editorial” was mainly based on the pantoprazole study and there was a surprising lack of biological, physiological and pathological aspects. Therefore, I wrote a letter to the “Editor” commenting on these shortcomings making the “Editorial” flawed. After two weeks I got a refusal from “The Editor-in-Chief” claiming that my letter was not relevant and without importance.

Generally, I mean that journals have an obligation to print letters showing imperfection, and that this obligation is particularly high for an editorial in the most prestigious journal of gastroenterology on a subject with implications for many patients. The clinicians should be able to read opposing views and thus make their own decision. I therefore publish my refused letter in this way.