KLF5 and posterior cortical atrophy: We deleted the endogenous KLF5 to generate KLF5-null (KLF5–/–) PC-3, DU 145, and C4-2B cells by introducing deletions that lead to early termination using the CRISPR-Cas9 system (Supplementary Fig. 3a–f), and then stably expressed empty vector (EV), wild-type KLF5 (KLF5), KLF5KR (KR), and KLF5KQ (KQ; Supplementary Fig. 3g) to establish PCa cells with different KLF5 acetylation statuses.