In support of this, we observed in that study that treatment of NPC cells with the PKC activator phorbol-12-myristate-13-acetate (PMA) increased levels of soluble vimentin and ameliorated the NPC lipid storage phenotype, whereas conversely, treatment of WT cells with PKC inhibitors resulted in the disappearance of soluble vimentin in those cells. The gene discussed is VIM; the disease is nasopharyngeal carcinoma.