CX3CR1 and prostate cancer: The addition of AZD8797 and JMS-17-2 selectively suppressed the growth of organoids with deAc-KLF5 (Figure 8E and Supplemental Figure 8A), indicating that induced Cx3cr1 by Klf5KR knockin is an essential mechanism by which Pten-deficient prostate cancer cells have an advantage in tumor growth.