GLI1 and posterior cortical atrophy: Given that NF-κB and SHh-GLI1 pathways sustain cell proliferation in advanced PCa and based on our findings demonstrating the existence of an active crosstalk between these two pathways, we hypothesized that the co-inhibition of NF-κB and SHh-GLI1 pathways could be a new potential therapeutic approach to treat PCa with constitutive activation of the NF-κB/GLI1 axis.