In this study, we report that CDK13 is significantly upregulated in PCa, and transcriptional activation of endogenous CDK13 promotes E2F5 expression by facilitating the formation of circCDK13, which in turn sponges miR-212-5p/449a and thus relieves their repression of the E2F5 expression, subsequently leading to the upregulation of E2F5 expression. The gene discussed is E2F5; the disease is posterior cortical atrophy.