Among the various dysregulated pathways, the Janus kinase/signal transducer and activator of transcription (JAK-STAT) signaling cascade has been recognized as a critical mediator of tumor progression, particularly through STAT3, which promotes proliferation, angiogenesis, immune suppression, and epithelial–mesenchymal transition (EMT) [33,34]. This evidence concerns the gene STAT3 and neoplasm.