The persistent activation of STAT3 in cancer can be counteracted by various mechanisms such as (i) inhibition of receptors leading to STAT3 activation; (ii) inhibition of ligand binding to STAT3 activating receptor; (iii) inhibition of the phosphorylation of the cytoplasmic tail of the receptor; (iv) inhibition of JAK kinases to cease STAT3 dimerization; and (v) prevention of its nuclear translocation and binding to specific response elements on DNA [68,69,70]. Here, STAT3 is linked to cancer.