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Disease tolerance describes an infected host's ability to maintain health independently of the ability to clear microbe loads. The Jak/Stat pathway plays a pivotal role in humoral innate immunity by detecting tissue damage and triggering cellular renewal, making it a candidate tolerance mechanism. Here, we find that in Drosophila melanogaster infected with Pseudomonas entomophila disrupting ROS -producing dual oxidase (duox) or the negative regulator of Jak/Stat Socs36E, render male flies less tolerant. Another negative regulator of Jak/Stat , G9a - which has previously been associated with variable tolerance of viral infections – did not affect the rate of mortality with increasing microbe loads compared to flies with functional G9a , suggesting it does not affect tolerance of bacterial infection as in viral infection. Our findings highlight that ROS production and Jak/Stat signalling influence the ability of flies to tolerate bacterial infection sex-specifically and may therefore contribute to sexually dimorphic infection outcomes in Drosophila. • The Jak/Stat pathway impacts disease tolerance during systemic infection with Pseudomonas entomophila. • Disrupting Duox or Socs36E render males less tolerant to systemic bacterial infection. • G9a does not affect tolerance during bacterial infection as it does during viral infection. [ABSTRACT FROM AUTHOR]