These results highlight a possibility that some avirulence effectors promote cell growth in the host while some virulence effectors play a suppressing role. It would be useful to identify additional PAMPs and the effectors of P. syringae that regulate cell fate determination in Arabidopsis in order to better understand the molecular mechanisms underlying cell fate control during Arabidopsis-P. syringae interactions. How are the signals from pathogens, such as bacterial flagellin, other PAMPs, and/or effectors, are transmitted to regulate host cell growth? One possibility is to perturb cell cycle progression, resulting in endoreplication and subsequently enlarged cells. Indeed, several cell cycle related genes are activated during host-pathogen interactions. In addition, several components of Anaphase Promoting Complex that represents a check point of cell cycle progression, were recently shown to play a role in defense control. Consistent with this speculation, we show here that enlarged cells have increased DNA content, a likely consequence of endoreplication. Fusion of plant cells in the infected region could also result in an increase in DNA content of the enlarged cells. However, we have not observed any morphological evidence to illustrate the cell fusion process. Pathogens could also regulate cell fate via manipulating host hormones. For instance, A. tumefaciens harbors genes encoding enzymes for the biosynthesis of cytokinins and auxin, which can be expressed in the host to perturb hormonal profile and subsequently induce crown galls in the infected Danshensu plants. Manipulating SA signaling is also a potential way to affect host cell fate. SA-dependent cell fate change has been reported in several defense mutants with lesion mimic phenotypes. Here we show that activation of SA signaling is necessary but not sufficient to induce cell enlargement in Arabidopsis. Thus, SA and an additional signal, potentially induced by pathogen infection, are required to regulate host cell fate change. It would be interesting to further elucidate what these additional signaling components are and how they affect host cell fate determination during Arabidopsis-P. syringae interaction. Why should hosts form enlarged cells upon pathogen attack? The enlarged cells often have higher nuclear DNA content and perhaps also increased metabolic activities. Thus they might confer a higher capacity to plant cells to respond to the accumulation of mutations and/or adverse stresses or 
to provide better nutrient reservoir for plant cells to increase their sizes. On the other hand, the rich nutrient reservoir can be hijacked by some pathogens that feed on these cells. Thus, these large cells can be the battleground during plant-pathogen interactions. The formation of large cells has been suggested as a susceptible response of hosts in several plant pathosystems. Here we show that during Arabidopsis-P. syringae Lomitapide Mesylate interactions, abnormal growths are induced more abundantly during PTI and ETI but not during ETS. In particular, we found that the large cells have thicker cell wall, possibly imposing a physical barrier to prevent further infection of pathogens. Such cell wall thickening of large cells induced by PTI is consistent with previous studies showing that PAMPs induce expression of genes involved in cell secretion and cell wall modification. Therefore, we propose that large cell formation might be a resistant response during Arabidopsis-P. syringae interactions. There are still many unanswered questions regarding cell fate control during host-pathogen interactions, a topic that warrants further investigations in order to yield a better understanding of mechanisms of cell fate control and disease resistance in plants.