Further RIP assays revealed that the KH3‐4 di‐domain of IGF2BP2 specifically bound to PCAT6 (Figure 4H), which indicated that the KH3‐4 domain was indispensable for the interaction between PCAT6 and IGF2BP2. Moreover, PCAT6 knockdown showed little effect on IGF2BP2 protein levels in PCa cells (Figure 4I), indicating that the interaction between PCAT6 and IGF2BP2 had no effect on the IGF2BP2 protein itself and IGF2BP2 was not the downstream target of PCAT6. This evidence concerns the gene PCAT6 and posterior cortical atrophy.