In breast cancer cells, E2 induces NGB upregulation and accumulation into mitochondria via the estrogen receptor α (ERα)-activated protein kinase B (AKT) pathway; this leads to the inhibition of the proteasome- and lysosomal-mediated NGB degradation, augmenting the phosphorylation of the nuclear transcription factor CREBP that is responsible for the transcription of the NGB gene [6]. The gene discussed is NGB; the disease is breast carcinoma.