The JNK dephosphorylation and deactivation rate of cells exposed to PETIC was reduced by PEITC directly downregulating the expression level of DUSP8 via proteasome-dependent mechanism, suggesting that PEITC targeting DUSP8, similar as a oncogene in prostate cancer, could restore activity of JNK through inhibiting the expression and activation of DUSP8 [75]. Here, DUSP8 is linked to prostate carcinoma.