We hypothesize that there is a homeostasis function of STAT1α and STAT1β in the normal situation, which TGF-β1 activates both sites (Y701 and S727); whereas there is abnormal higher level of STAT1 in a tumor cell, which TGF-β1 increases the phosphorylation of STAT1 at S727 site (STAT1α) and decreases the phosphorylation of STAT1 at Y701 site (STAT1α/β). Here, STAT1 is linked to neoplasm.