The cost of a plant deploying its defences against invading pathogens has been linked to altered photosynthesis, respiration or metabolite deficiency as resources are diverted towards defence. The defence responses have also been shown to alter stomatal function. During resistance responses to powdery mildew pathogens mediated by R genes in barley and oats, stomata lock in an open configuration, displaying little or no closure in response to diurnal rhythms or abscisic acid. As a result, these plants exhibit compromised tolerance to drought. Conversely, in response to rust fungal pathogens, major gene resistance is linked to stomata locking shut which has severe impacts on gas exchange, and causes photosynthetic disruption through the over-reduction of redox-active components and poorer cooling via the transpirational stream. Thus, stomatal locking probably results in a yield cost of resistance particularly in locations with higher light levels and/or prone to drought, and it is therefore imperative to define their underlying mechanisms. This paper reviews the effects of different types of resistance and their signalling cascades on stomatal function, including effector-triggered immunity (defence based on R genes), PAMP-triggered immunity and responses to toxins. More widely, it considers whether stomatal dysfunction could be a feature of wider changes in primary metabolism where regulation of osmolytes is disrupted. This would integrate stomatal locking as one feature of the wider cost of resistance. As such, reduced stomatal lock-up could be used as a readily measureable marker for lines with a reduced resistance penalty.