It is suggested that sustained activation of androgen-receptor (AR) signaling in CR disease [7], activation of alternative oncogenic survival pathways (such as EGFR, PI3K/Akt, MAPK/ERK) [8, 9] and overexpression of βIII-tubulin and/or drug efflux proteins [10, 11] could underlie the DTX therapeutic failure in PCa. Here, AR is linked to posterior cortical atrophy.