Thus, based on our hypothesis that CD56 is a predictive biomarker for responsiveness to NK-92-mediated cytotoxicity, if adoptive NK-92 transfer is to be used in breast cancer patients, we would expect, unresponsiveness in more than two-thirds of the cases (no or very low % of CD56 expressing cells), and at best, very low responsiveness with rapid relapse in 12.1% of the cases (high intratumoral heterogeneity regarding CD56 expression; 30–69% CD56-positive cells) and better responsiveness with longer RFS in 24.2% of the cases (70–100% of CD56-positive cells per tissue). This evidence concerns the gene NCAM1 and breast carcinoma.