Recent progress in the field extend these well-known functions and place these isoforms in the center of a comprehensive regulatory network controlling major epithelial-to-mesenchymal transition (EMT)-relevant signaling pathways [such as transforming growth factor-β (TGF-β), wingless-int (WNT), insulin-like growth factor (IGF), and signal transducer and activator of transcription (STAT)), microRNAs, and EMT-associated transcription factors that promote invasion, loss of tumor cell polarity, and metastatic behavior in conjunction with a chemo-resistant phenotype [77]. This evidence concerns the gene SOAT1 and neoplasm.