Recently, a BCLxL-specific PROTAC created from navitoclax that targets BCLxL to the Von Hippel-Lindau (VHL) E3 ligase for degradation was shown to be able to selectively kill various BCLxL-dependent cancer cells with higher potency than venetoclax but significantly lower platelet toxicity due to minimal expression of VHL in platelets [142]. The gene discussed is VHL; the disease is cancer.