Lately, an appraisal of evidence on NGAL dysregulation in cancer has described the concept of NGAL overexpression resulting from hypoxic and inflammatory stimuli (potentially via active nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) pathways) originating from the tumor microenvironment. The gene discussed is LCN2; the disease is cancer.