EED and posterior cortical atrophy: Taken together, these mechanistic studies supported a working model that LG1980 may interrupt the EED-EZH2 interaction, disassemble the PRC2 complex, destabilize core PRC2 components (EED, EZH2, and SUZ12) and reduce the level of p-EZH2(S21), thereby selectively inhibiting the noncanonical EZH2-Stat3-SKP2-ABCB1/survivin signaling and inducing apoptosis in chemoresistant PCa cells (Figure 5D).