Xathomonas citri subsp. citri causes citrus canker disease worldwide in most commercial varieties of citrus. Its transmission occurs mainly through wind-driven rain. Once on the leaf X. citri can epiphytically survive forming biofilm, which enhances persistence of the bacteria to different environmental stresses and play an important role in the early stages of host infection. Therefore, the study of genes involved in biofilm formation has been an important step towards the understanding of the bacterial strategy to survive and infect the plant host. In this work we show that ecnAB a Toxin-Antitoxin (TA) system, previously identified only in human bacterial pathogen, is conserved in many Xanthomonas spp. In general TA systems consist of a pair of genes in operon that encodes a stable toxin and an unstable antitoxin that, under normal conditions, binds to the toxin and blocks its activity. On the other hand, under stress the antitoxin is degraded, allowing the toxin to act decreasing cell growth and metabolism. When normal growth conditions are re-established, the antitoxin is produced, blocking the toxin and allowing the cells to grow. Thus, this mechanism represents an important bacterial strategy of survival under stress conditions. In this work, we show that in X. citri ecnAB is regulated by quorum sensing and it is involved in important processes such as biofilm formation, EPS production, and motility. In addition, we show that ecnAB plays a role in X. citri survival and virulence in plant host.