Interestingly, treatment with a broad spectrum inhibitor of protein kinase C (PKC) enzymes, which are known upstream activators of CARD14 family proteins [43], not only failed to inhibit NF-κB/JNK/Akt phosphorylation, but also MALT1-mediated CYLD and A20 cleavage (Figure 5A), suggesting that constitutive CBM activation in PCa cells is mediated by a PKC-independent mechanism. The gene discussed is CYLD; the disease is posterior cortical atrophy.