Molecular changes that correlate with acquired therapy resistance to taxane medication include tubulin alterations, overexpression of ERG, increased expression of the transporter ABCB1, and up-regulation of the glucocorticoid (GR) and AR networks.11, 12, 13 Elevated GR expression is a potential driver of therapy resistance, and it accelerates PCa tumor progression.14, 15, 16 In addition, PCa cells show increased intratumoral steroidal, cholesterol, and lipid synthesis, which contributes to the decreased efficacy of antiandrogens and chemotherapy.17 This evidence concerns the gene ERG and posterior cortical atrophy.