The possible relevance of miR-205 for PCa radiation response is based on our previous observation that its reconstitution in PCa cells counteracts EMT [17] and increases the antitumor activity of the DNA damaging agent cisplatin in vitro and in vivo, as a consequence of autophagy impairment [22], as well as on the reported evidence that PKCε, a direct miR-205 target [17], plays a role in the nuclear translocation of EGFR, which is lost upon PKCε knockdown thus impairing DNA-double strand break (DSB) repair [23]. The gene discussed is PRKCE; the disease is posterior cortical atrophy.