Interestingly, pharmacological inhibition of PKC activity, in addition to reducing HuR phosphorylation at serine 318, had a strong inhibitory effect on the high cytoplasmic HuR abundance [107], thus, implying the high constitutive HuR phosphorylation may be causative for the pathologically-increased cytoplasmic HuR levels observed in tissue specimens from CRC patients or patients with early adenomas or inflammatory bowel diseases [10]. The gene discussed is ELAVL1; the disease is adenoma.