Moreover, similar to that of the overexpression or mutation of receptor tyrosine kinase, most cancers, including breast cancer-associated lesions, that lead to constitutive or uncontrolled activation of ERK signaling (55) were due to either the overexpression of IL-17A/IL-17RA and ACT1-TRAF-6 or the activating mutation of TAK-1 molecule (63, 76, 77). This evidence concerns the gene IL17RA and breast carcinoma.