Interestingly, Ub‐K6R mutation almost abolished the signals (percent and MFI) of FOXA1 ubiquitination (Fig. 2K) compared to Ub‐K29R mutation, suggesting that K6‐ and K29‐linked polyubiquitination may not play equivalent roles in the SKP2‐mediated polyubiquitination of FOXA1 in PCa. This evidence concerns the gene FOXA1 and posterior cortical atrophy.