Choi et al. (2017) demonstrated that TM4SF4 was involved in epithelial mesenchymal transition (EMT) and cancer stem cell (CSC) properties of non-small cell lung cancer (NSCLC) through the regulation of osteopontin. TM4SF4 triggered OPN expression by creating a positive feedback autocrine loop with JAK2/STAT3 or focal adhesion kinase (FAK)/STAT3 pathways. Blocking the activity of TM4SF4 using specific antibody and short interfering RNA (siRNA) can be a promising therapeutics against TM4SF4-overexpressing cancer (Wang et al., 2013; Choi et al., 2014). The gene discussed is STAT3; the disease is cancer.