Assessment of prognosis on the basis of molecular characteristics would help inform decisions and tailor therapy to ESCC individuals so as to achieve the best possible outcome. Our survival analysis revealed that downregulation of 14-3-3s was significantly correlated with poor prognosis of ESCC. Thus, patients with reduced expression of 14-3-3s had a significantly lower 5-year survival rate relative to ESCC patients with a high level of 14-3-3s expression. Multivariate analysis found that 14-3-3s was an independent prognostic factor for ESCC. Other studies form China support the current findings, but a study form Japan reported that overexpression of 14-33s in the nucleus was a poor prognosis factor. Esophageal carcinogenesis is a complex dynamic biological process involving a myriad of molecular alternations in a multi-stage evolution. It seems unlikely therefore that a single gene expression could suffice to predict the prognosis of ESCC. As such, SVM was used to build a reliable ESCC classifier on the basis of clinicopathological features and 14-3-3s expression to improve the accuracy of prognostication. The predictive accuracy of our ESCC classifier incorporating sex, age, T stage, histological grade, lymph node metastasis, clinical stage and 14-3-3s expression was better than any individual component. The last few years have witnessed a surge of research on the study of the physiological function and in vivo substrates of the fat mass and obesity associated gene. Recent interest in the FTO gene stems from studies demonstrating an association between a single nucleotide polymorphism in the first intron of the gene with obesity-related traits and higher obesity risk in different human populations. From a molecular point of view, FTO has been characterized as a 2-oxogluterate dependent dioxygenase that is involved in nucleic acid modification. In mice, global deletion of FTO has been linked to postnatal growth retardation, reduction in adipose tissue, reduction in lean mass and increased energy expenditure, thus supporting the involvement of FTO in energy metabolism and body weight regulation. FTO is ubiquitously expressed. In the brain, strong expression is seen in the hippocampus, cerebellum and hypothalamus. The hypothalamic expression of FTO suggests a potential role of this gene in the regulation of autonomic function. The paraventricular and dorsomedial nuclei of the hypothalamus, which show particularly high expression of FTO, are key modulators of sympathetic outflow. Interestingly, preliminary evidence seems to connect FTO deficiency in mice with increased sympathetic nervous system activity. FTO is also expressed in many other tissues including the heart, albeit at substantially lower levels. Given these considerations, the principal objective of the present study was to investigate the potential role of the FTO gene in the autonomic neural regulation of cardiac function.