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Plants face many biotic and abiotic challenges in nature; one of them is attack by disease-causing microbes. <i>Phytophthora infestans</i>, the causal agent of late blight is one of the most prominent pathogens of the potato responsible for multi-billion-dollar losses every year. We have previously reported that potato-associated <i>Pseudomonas</i> strains inhibited <i>P. infestans</i> at various developmental stages. A comparative genomics approach identified several factors putatively involved in this anti-oomycete activity, among which was the production of hydrogen cyanide (HCN). Here, we report the relative contribution of HCN emission to the overall anti-<i>Phytophthora</i> activity of two cyanogenic <i>Pseudomonas</i> strains, <i>P. putida</i> R32 and <i>P. chlororaphis</i> R47. To quantify this contribution, we generated HCN-negative mutants (Δhcn) and compared their activities to those of their respective wild types in different experiments assessing <i>P. infestans</i> mycelial growth, zoospore germination, and infection of potato leaf disks. Using in vitro experiments allowing only volatile-mediated interactions, we observed that HCN accounted for most of the mycelial growth inhibition (57% in R47 and 80% in R32). However, when allowing both volatile and diffusible compound-mediated interactions, HCN only accounted for 1% (R47) and 18% (R32) of mycelial growth inhibition. Likewise, both mutants inhibited zoospore germination in a similar way as their respective wild types. More importantly, leaf disk experiments showed that both wild-type and Δhcn strains of R47 and R32 were able to limit <i>P. infestans</i> infection to a similar extent. Our results suggest that while HCN is a major contributor to the in vitro volatile-mediated restriction of <i>P. infestans</i> mycelial growth, it does not play a major role in the inhibition of other disease-related features such as zoospore germination or infection of plant tissues.