Given that SHh and NF-κB(p65) control genes that are involved in several altered processes in PCa, and that SHh is a transcriptional target of NF-κB(p65) [33], we investigate the role of the NF-κB(p65)-SHh-GLI1 axis in a specific subset of advanced PCa, with the aim to identify novel molecular targets for future CRPC therapies. This evidence concerns the gene NFKB1 and posterior cortical atrophy.