During normoxia, oxygen-sensing HIF-1α is hydroxylated and degraded via the proteasome, whereby under hypoxic conditions, hydroxylation is impaired due to oxygen shortage, resulting in HIF-1α stabilization, its nuclear translocation, and subsequent transcription of target genes related to angiogenesis, glycolysis, migration, and tumor progression, also via crosstalk with other pathways, such as NFκB [28]. This evidence concerns the gene NFKB1 and neoplasm.