Zou et al. showed that endogenous PKD2 interacted with and phosphorylated IKKβ in invasive prostate cancer cells and was responsible for the nuclear translocation and activation of the p65 subunit of NF-κB through phosphorylation of S276 on p65, whereas PKD3 was responsible for S536 phosphorylation on p65 and deactivation of HDAC1 [83]. This evidence concerns the gene PRKD3 and prostate cancer.