As before, the PROTACs demonstrated marked improvement in efficacy over the inhibitor alone, as was seen for PROTAC-3 (VHL-defactinib) which showed superiority over clinical candidate defactinib (Fak inhibitor only) in Fak inactivation and impediment of Fak mediate prostate tumor cell line (PC3) invasion [50]. The gene discussed is PTK2; the disease is prostate neoplasm.