Although TET2 is less frequently mutated in primary PCa as compared to metastatic PCa, several factors have been hypothesized as potentially contributing to its loss of expression, including hypoxia, which deprives TET enzymes of the oxygen required for their dioxygenase activity, alterations in expression of TET-governing transcription factors such as high-mobility group AT-hook 2 (HGMA2), and repression of TET by oncogenic miRNAs [25, 28]. Here, TET2 is linked to posterior cortical atrophy.