Experimental evidence suggests that TH could support the estrogen-dependent proliferation of BC cells in several ways: (i) TH may increase the expression of estrogen receptors (ERs) [108,109]; (ii) TRE and the ER response element (ERE) share an identical half-site, and THRs have been shown to bind also to ERE [110]; (iii) thyroxine, through the αvβ3 integrin receptor, may activate MAPK signaling and the phosphorylation of the nuclear ERα [111]. This evidence concerns the gene ESR1 and breast cancer.