The ascomycete fungus Verticillium dahliae causes vascular wilt diseases in hundreds of dicotyledonous plant species. However, thus far, only few V. dahliae effectors have been identified, and regulators of pathogenicity remain unknown. In this study, we investigated the role of the V. dahliae homolog of Sge1, a transcriptional regulator that was previously implicated in pathogenicity and effector gene expression in Fusarium oxysporum. We show that V. dahliae Sge1 (VdSge1) is required for radial growth and production of asexual conidiospores, because VdSge1 deletion strains display reduced radial growth and reduced conidia production. Furthermore, we show that VdSge1 deletion strains have lost pathogenicity on tomato. Remarkably, VdSge1 is not required for induction of Ave1, the recently identified V. dahliae effector that activates resistance mediated by the Ve1 immune receptor in tomato. Further assessment of the role of VdSge1 in the induction of the nine most highly in-planta-induced genes that encode putative effectors revealed differential activity. Although the expression of one putative effector gene in addition to Ave1 was not affected by VdSge1 deletion, VdSge1 appeared to be required for the expression of six putative effector genes, whereas two of the putative effectors genes were found to be negatively regulated by VdSge1. In conclusion, our data suggest that VdSge1 differentially regulates V. dahliae effector gene expression.