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During host plant infection, pathogens produce a wide array of cell wall degrading enzymes (CWDEs) to break the plant cell wall. Among CWDEs, xylanases are key enzymes in the degradation of xylan, the main component of hemicellulose. Targeted deletion experiments support the direct involvement of the xylanase BcXyn11a in the pathogenesis of <i>Botrytis cinerea</i>. Since the <i>Triticum aestivum</i> xylanase inhibitor-I (TAXI-I) has been shown to inhibit BcXyn11a, we verified if TAXI-I could be exploited to counteract <i>B. cinerea</i> infections. With this aim, we first produced <i>Nicotiana tabacum</i> plants transiently expressing TAXI-I, observing increased resistance to <i>B. cinerea</i>. Subsequently, we transformed <i>Arabidopsis thaliana</i> to express TAXI-I constitutively, and we obtained three transgenic lines exhibiting a variable amount of TAXI-I. The line with the higher level of TAXI-I showed increased resistance to <i>B. cinerea</i> and the absence of necrotic lesions when infiltrated with BcXyn11a. Finally, in a droplet application experiment on wild-type <i>Arabidopsis</i> leaves, TAXI-I prevented the necrotizing activity of BcXyn11a. These results would confirm that the contribution of BcXyn11a to virulence is due to its necrotizing rather than enzymatic activity. In conclusion, our experiments highlight the ability of the TAXI-I xylanase inhibitor to counteract <i>B. cinerea</i> infection presumably by preventing the necrotizing activity of BcXyn11a.