Prostate cancer cells resistant to androgen deprivation (AD) therapy were characterized by elevated FOXC2, the associated EMT/CSC phenotype and increased drug resistance, which were related to the activation of p38 MAPK signaling, a key pathway in promoting cell survival and proliferation[133].The study of the mechanism suggested that FOXC2 augmented p38 phosphorylation[133]. This evidence concerns the gene FOXC2 and prostate carcinoma.