Considering the well-known features of ANXA2 as an adhesion molecule and chemoattractant for PCa cells [37], Shiozawa et al. [22] proposed that the lack of ANXA2 in the primary tumor could exert selective pressure over prostatic cancers favoring not only the detachment of cells from the primary tumor, but also the migration to the bone, a niche rich in ANXA2. This evidence concerns the gene ANXA2 and posterior cortical atrophy.