The bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), is the most important disease of kiwifruit, threatening its production in the world. However, little is known about the molecular interaction between Psa and kiwifruit plants. To elucidate early molecular plant response during the different phases of the infection, gene expression in healthy or inoculated plants of Actinidia chinensis was analyzed 3, 24 and 48 h after experimental inoculation. Moreover, to understand the molecular mechanism underlying the increased plant resistance observed after the exogenous application of the SAR inducer acibenzolar-S-methyl (ASM), gene expression was analyzed in healthy or inoculated AMS pre-treated plants. The inoculation was done with Psa carrying the green fluorescent protein gene (gfp, allowing to check bacterial colonization by confocal laser scanning microscopy. Transcriptome analysis of A. chinensis, was performed using an Illumina GAIIx sequencer, generating 221 millions 75 bp long paired end reads. The raw reads were de novo assembled into 52,811 contigs by Trinity software with an average size of 988 bp and N50 of 1,510 bp. Annotation of the de-novo transcript contigs was done using Blast2GO software. BLASTx and BLASTn were performed against the NR protein, RefSeq protein and SwissProt/UniProt databases and against NR nucleotide database, respectively, with an E-value cut-off of 1e-5. The BLASTx matches was used for further GO mappings to give a putative functional annotation to contigs. The functionality InterProScan in Blast2GO software allowed to retrieve domain/motif information in the InterPro and in other domain databases (i.e. Pfam, SuperFamily). Furthermore local BLASTx alignments was made against the Clusters of Orthologous Groups (COGs) database. Reads were mapped to the contigs using the CLC software to identify differentially expressed genes (DEGs), statistical analysis was done using the method described in the R package DESeq. A preliminary analysis of DEGs was conducted on sequences obtained at 24h after infection. 328 DEGs were identified in response to infection in plants not pre-treated with ASM. When ASM pre-treated plants were considered, 564 DEGs were identified, 202 of them were in common with the 328 DEGs modulated by infection in not ASM pre-treated plants. The ASM treatment per se (without infection) was able to modulated 1,043 DEGs, 109 of them were further modulated by infection in ASM pre-treated plants. These results suggest that the molecular response to Psa is strongly enhanced in ASM pre-treated plants. Additional data analysis are in progress