Gastric cancer (GC) is a multifactorial disease, which can be triggered by numerous factors, including Helicobacter pylori infection, genetic susceptibility, and environmental factors. GC develops from the accumulation of multiple genetic and epigenetic alterations in oncogenes and tumor suppressor genes. In this article, we review the literature published in the past year regarding GC genomic and epigenetic characteristics associated with cancer biology. With advances in high-throughput sequencing techniques, many studies have undertaken the molecular profiling of GCs and a large number of non-coding transcripts from regions previously termed “junk DNA”. Long non-coding RNAs and circular RNAs are representative non-coding RNAs that fill a significant gap that was previously unknown or not well understood in the field of gastric carcinogenesis. The study of lncRNA has gone beyond the level of mechanistic studies to clinically relevant studies, indicating its usefulness as a biomarker. Understanding the molecular characteristics of GC is very important for deciding treatment strategies, such as target agents and immunotherapy. Therefore, research analyzing tumor behavior at the molecular level plays a pivotal role in dissecting GC heterogeneity. In this review, we summarize the most recent research updates on the role and function of the gastric microbiota in the process of carcinogenesis. While there is little evidence regarding the drivers or modifiers in the gastric microbiota that mediate the development of GC, many studies have identified gastric microbiota players associated with gastric carcinogenesis and have presented these as candidate targets for therapeutic interventions.