In particular, they showed that growth of AR-negative PCa may be driven by a DOT1L-HES6 fusion gene, originating by an interchromosomal rearrangement that fused intron 9 of DOT1L with a position 4 kb upstream of HES6, resulting in overexpression and pathological activation of this gene, encoding a transcription factor representing a key player in the induction of castration-resistant PCa (Annala et al., 2014). Here, AR is linked to posterior cortical atrophy.