The analysis showed that the transgene and the miniprotein significantly modulated gene sets that confirm shutdown of the MYC fingerprint (downregulation of MYC targets) and can explain its antitumor and antimetastatic activity observed in vitro and in vivo (downregulation of cell-cycle progression, EMT and breast cancer grade, and upregulation of tumor rejection genes, among many others; Fig. 6A and B). Here, MYC is linked to breast cancer.