Collectively, these results indicate that GLIPR1-ΔTM may be a good candidate for combination therapy with docetaxel, since it promotes PCa specific cell death through JNK activation, whereas it downregulates c-Myc signaling which has been extensively associated with the emergence of resistance to docetaxel through ERK1/2-c-Myc-CXCR4 signaling. This evidence concerns the gene MAPK3 and posterior cortical atrophy.