In cancer, dysregulation of Jab1/COPS5 expression may originate from three regulatory mechanisms: gene amplification, microRNAs, and other signaling transduction pathways such as IL6-Stat3 (signal transducer and activator of transcription 3) signaling, HER2-AKT (human epidermal growth factor receptor 2-protein kinase B) signaling, and BCR-ABL signaling. The gene discussed is AKT1; the disease is cancer.