Blackleg disease of Brassica napus caused by Leptosphaeria maculans (Lm) is largely controlled by deploying race-specific resistance (R) genes. However, selection pressure exerted by R genes causes Lm to adapt and give rise to new virulent strains through mutation and deletion of effector genes. Therefore, knowledge of effector gene function is necessary for effective management of the disease. Here we report cloning of Lm effector AvrLm9 that is recognised by the resistance gene Rlm9 in B. napus cultivar Goéland. AvrLm9 was mapped to scaffold 7 of Lm genome, co-segregating with the previously reported AvrLm5 (previously known as AvrLmJ1). Comparison of AvrLm5 alleles among the 37 re-sequenced L. maculans isolates and transgenic complementation identified a single point mutation correlating with the AvrLm9 phenotype. Therefore we renamed this gene as AvrLm5-9 to reflect the dual specificity of this locus. Avrlm5-9 -transgenic isolates were avirulent when inoculated on the B. napus cultivar Goéland. Expression of AvrLm5-9 during the infection was monitored by RNA-sequencing. Recognition of AvrLm5-9 by Rlm9 is masked in the presence of AvrLm4-7, another Lm effector. AvrLm5-9 and AvrLm4-7 do not interact, and AvrLm5-9 is expressed in the presence of AvrLm4-7. AvrLm5-9 is the second Lm effector for which host recognition is masked by AvrLm4-7. Understanding this complex interaction will provide new opportunity for engineering broad-spectrum recognition. This article is protected by copyright. All rights reserved.