Activation of phF1.6 by Tax-1 and Tax-2 could be attributed to classical NF-κB signaling: (1) inhibition of IKK2 by a chemical compound [69,70], (2) inhibition of IκB by co-transfection of a dominant-negative inhibitor [54], and, in case of Tax-1, (3) NF-κB-deficient Tax-mutants [71], led to decreased Tax-mediated transactivation of the Fascin promotor ([41]; this work), which is in line with earlier observations in human breast cancer cell lines [72,73]. Here, CNTN2 is linked to breast cancer.