In certain mouse models of CRC, inhibiting phosphorylated c-Jun or colon-specific c-Jun inactivation has shown to reduce tumor burden and extend lifespan.90 In addition, JNK1 has been identified as an upstream regulator of Stat3 and has been implicated in other anticancer mechanisms, including the inhibition of centrosomal amplification.91 This evidence concerns the gene STAT3 and colorectal carcinoma.