Dear Editor, Gastric cancer represents a remarkable disease burden worldwide, ranking among the first five tumor types in incidence and mortality [1]. Germline DNA variation has been extensively investigated in terms of predisposition to sporadic gastric cancer, which represents more than 90% of all cases [2]. Currently available evidence shows that the fraction of disease burden that can be attributable to known risk polymorphisms is small (< 20%)[2]. Single germline variations of circadian genes (also called clock genes) have been associated with the predisposition of different tumor types [3]. The circadian clock is a timetracking rhythmic biological system with a periodicity of about 24 hours that enables organisms to anticipate environmental changes and allow them to modify their behavior and physiological functions in the most efficient way. Circadian rhythms are controlled by proteins encoded by circadian genes, which have been discovered in all studied species. Remarkably, the disruption of these rhythms has been linked with risk of different diseases including cancer. In regards to the latter, a growing wealth of evidence supports the potential tumor suppressor role of the biological clock [3, 4]. As the role of circadian gene germline variants has never been explored in the field of gastric cancer susceptibility, with the present work, we intended to test the hypothesis that specific single nucleotide polymorphisms (SNPs) of the circadian genes, such as CLOCK, NPAS2, PER1, PER2, RORA, and TIMELESS, could significantly increase or decrease the predisposition to develop gastric cancer. We considered the 10 SNPs of the above listed 6 circadian genes that are known to be functional or associated with cancer risk or prognosis. The main features of the SNPs are described in our previous study [5].