In a systematic review, Isali and colleagues (2020) provided insight into the genetic pathogenesis of SUI by gathering and synthesizing the available data from studies evaluating differential gene expression in SUI patients and identified possible novel therapeutic targets and leads. A systematic literature search was conducted through September 2017 for the concepts of genetics and SUI. Gene net-working connections and gene-set functional analyses of the identified genes as differentially expressed in SUI were performed using GeneMANIA software. Of 3,019 studies, 4 were included in the final analysis. A total of 13 genes were identified as being differentially expressed in SUI patients; 11 genes were over-expressed: skin-derived antileukoproteinase (SKALP/elafin), collagen type XVII alpha 1 chain (COL17A1), plakophilin 1 (PKP1), keratin 16 (KRT16), decorin (DCN), biglycan (BGN), protein bicaudal D homolog 2 (BICD2), growth factor receptor-bound protein 2 (GRB2), signal transducer and activator of transcription 3 (STAT3), apolipoprotein E (APOE), and Golgi SNAP receptor complex member 1 (GOSR1), while 2 genes were under-expressed: fibromodulin (FMOD) and glucocerebrosidase (GBA). GeneMANIA revealed that these genes are involved in intermediate filament cytoskeleton and extra-cellular matrix organization. The authors concluded that many genes are involved in the pathogenesis of SUI. Furthermore, whole-genome studies are needed to identify these genetic connections. These researchers stated that this study laid the groundwork for future research and the development of novel therapies and SUI biomarkers in clinical practice.