The Asian soybean rust fungus, Phakopsora pachyrhizi, is an obligate biotrophic pathogen causing severe soybean disease epidemics. Molecular mechanisms by which P. pachyrhizi and other rust fungi interact with their host plants are poorly understood. The genomes of all rust fungi encode many small, secreted cysteine-rich proteins (SSCRP). While these proteins are thought to function within the host, their roles are completely unknown. Here, we present the characterization of P. pachyrhizi effector candidate 23 (PpEC23), a SSCRP that we show to suppress plant immunity. Furthermore, we show that PpEC23 interacts with soybean transcription factor GmSPL12l and that soybean plants in which GmSPL12l is silenced have constitutively active immunity, thereby identifying GmSPL12l as a negative regulator of soybean defenses. Collectively, our data present evidence for a virulence function of a rust SSCRP and suggest that PpEC23 is able to suppress soybean immune responses and physically interact with soybean transcription factor GmSPL12l, a negative immune regulator. Asian soybean rust is a disease caused by the rust fungus, Phakopsora pachyrhizi, which was first described in Japan in 1902 and eventually reached North and South America in the early 2000s. Like other rust fungi, P. pachyrhizi, is capable of causing disease epidemics that severely reduce crop yields. Rust fungi require living host tissue in order to complete their life cycles, and thus, we expect that they produce and secrete effector proteins that are transferred into plant cells to interfere with immune responses. Small proteins that are rich in the amino acid cysteine and predicted to be secreted have been proposed to be likely candidates for effector proteins. Here, we report that a secreted, small cysteine-rich protein from P. pachyrhizi suppresses plant immunity, and furthermore, it interacts with a soybean transcription factor protein. Interestingly, silencing of this transcription factor results in plants that have increased expression of defense marker genes and enhanced disease resistance, which demonstrates that it is a negative regulator of soybean immune responses. Our work shows that, indeed, a small cysteine-rich protein from a rust fungus can suppress plant immunity, and furthermore, it identifies a new function for SQUAMOSA PROMOTER BINDING-LIKE (SPL) transcription factors as components of the defense regulatory networks that holds immune responses in check.