Since the clinical drug development of the BCL-xL/2 dual inhibitor navitoclax has been hindered by dose-limiting and on-target thrombocytopenia due to BCL-xL inhibition in platelets [27,28,29], we have recently converted navitoclax into platelet-sparing BCL-xL PROTAC degraders using VHL E3 ligase for their activity, which significantly reduced platelet toxicity [32]. The gene discussed is VHL; the disease is Thrombocytopenia.