Interfering with NGAL activity in neoplastic and/or tumor stromal cells could be realized by different ways: knockdown of its expression by classical siRNA or CRISPR-Cas9 gene editing system, neutralization of its function by monoclonal antibodies raised against NGAL itself or its receptors, inhibition of siderophores binding by small selective inhibitors. Here, LCN2 is linked to neoplasm.