Summary The fungus Parastagonospora nodorum is the causal agent of Septoria nodorum blotch of wheat ( Triticum aestivum ). The interaction is mediated by multiple fungal necrotrophic effector–dominant host sensitivity gene interactions. The three best‐characterized effector–sensitivity gene systems are SnToxA– Tsn1 , SnTox1– Snn1 and SnTox3– Snn3 . These effector genes are highly expressed during early infection, but expression decreases as the infection progresses to tissue necrosis and sporulation. However, the mechanism of regulation is unknown. We have identified and functionally characterized a gene, referred to as PnPf2 , which encodes a putative zinc finger transcription factor. PnPf2 deletion resulted in the down‐regulation of SnToxA and SnTox3 expression. Virulence on Tsn1 and Snn3 wheat cultivars was strongly reduced. The SnTox1– Snn1 interaction remained unaffected. Furthermore, we have also identified and deleted an orthologous PtrPf2 from the tan spot fungus Pyrenophora tritici‐repentis which possesses a near‐identical ToxA that was acquired from P. nodorum via horizontal gene transfer. PtrPf2 deletion also resulted in the down‐regulation of PtrToxA expression and a near‐complete loss of virulence on Tsn1 wheat. We have demonstrated, for the first time, evidence for a functionally conserved signalling component that plays a role in the regulation of a common/horizontally transferred effector found in two major fungal pathogens of wheat.