MYC and gastric cancer: CagA also triggers inflammation and oxidative stress via various pathways, including IL-11/signal transducer and activator of transcription (STAT)-3/CDX2, c-Myc/p21/extracellular signal regulated kinase (ERK)-mitogen-activated protein kinase (MAPK), toll-like receptor, and reactive oxygen species/apoptosis signal regulating kinase-1/c-Jun N-terminal kinase signaling [21], which leads to DNA damage and genomic instability, ultimately increasing the risk of gastric cancer development.