Apple canker disease, caused byValsa mali, is one of the most serious apple tree diseases in China.VmSom1is an important transcription factor that acts on the cyclic adenosine signaling pathway (cAMP/PKA), regulating the growth, development, morphological differentiation, and pathogenic forces of the pathogen. We perform transcriptome analysis of theVmSom1deletion mutant and the wild-type strain 11-175 and identify a significantly differentially expressed gene,VM1G_06867, a zinc finger motif transcription factor inV. mali. In this study, we obtain theVM1G_06867gene using the single deletion mutant via homologous recombination. To determine the relationship betweenVmSom1andVM1G_06867, we also obtain a double deletion mutantΔVmSom1/06867. Compared to the wild-type strain 11-175, the single deletion mutantVM1G_06867shows a drastic reduction in growth rate and forms more pycnidia on the PDA medium. Additionally, the growth of the mutant is inhibited by SDS, Congo red, and fluorescent brighteners. In comparison to the single deletion mutantVmSom1, the double deletion mutantΔVmSom1/06867shows no significant change in growth or conidiation and is unable to produce conidia. The growth rate is significantly increased in Congo red, NaCl, and Sorbitol mediums. These results demonstrate thatVM1G_06867plays important roles in growth, pathogenicity, asexual development, and maintenance of cell wall integrity.VM1G_06867can recover osmotic stress and cell wall integrity defects caused by the deletion ofVmSom1, as well as restore the loss of pathogenicity caused by the deletion of theVmSom1gene, but not completely.