The infection of ToMV could have led to the alteration of the concentration gradient of sucrose in phloem. The plant overexpressed bfructofuranosidase to ensure the sucrose transport of source cells to the sink cells. Overexpression of invertase in tomato-virus interaction could be elicited by the expression of pathogenesis-related proteins and by salicylic acid in order to increase resistance to virus infection. In order to ensure the success of defense, this mechanism appears to be crucial. The phenomenon of “high sugar resistance” was described long ago and the finding that various pathogenesis-related genes were sugar-inducible supports this hypothesis. We also found six gibberellin, one SAM dependent carboxyl methyltransferase and one jasmonate-zim domain genes up-regulated, suggesting that GAs activated tomato immune responses to ToMV by modulating the levels of salicylic acid and/or jasmonic acid. Plants rely on the innate immunity and on systemic signals emanating from metabolic alterations. The ETI system seems to prompt response in the right direction thanks to metabolic clues and hormone signaling. Salicylic acid primarily triggers resistance against biotrophic pathogens, whereas a combination of jasmonic acid and ethylene signaling activates resistance to necrotrophic pathogens. The metabolic changes associated with defense response in two incompatible tomatopathogen interactions suggested that the response to the specific metabolic alteration in tomato was pathogen-specific and contributed substantially to monogenetic gene resistance. Our results confirm that resistance to pathogens depends on a sophisticated interplay among different biological pathways and that hormonal directionality is critical to the outcome of a response. Several hormones involved in pathogen perception, activation of defense products restricting pathogen invasion, have been identified. How they trigger ETI defense is currently unclear. In the absence of a pathogen, NB-ARC genes are in an autoinhibition state, which is relieved upon pathogen perception. Although different forms of plant immunity share the same signaling mechanisms, they use the same mechanisms in very different ways. The mechanisms that lead to rapid metabolism switch and connection among all the defense pathways is still not clear. Signaling able to fine-tune the defense mechanism could be activated by genes in proximity of the main pathogen receptors. Genome organization of functional gene networks to tolerate alterations can result in plasticity. In two specific interactions the chromosome distribution of expressed genes showed wide overlapping regions, except for the region holding genes I2 and Tm2. Indeed, genome regions can be enriched in genes with the specific function for fine-tuning gene expression in a compensatory way. In Fol interaction on chromosome 11 region harboring I2 gene a calmodulin gene, a myb factor and a BEL-l like homeodomain protein.