Moreover, despite the fact that the ubiquitin-proteasomal pathway emerges as an important regulator of c-FLIP expression in tumor cells,47 our results demonstrate that neither phosphorylation or ubiquitination of c-FLIP nor inhibition of the proteasome inhibited c-FLIP depletion from the cytosol during hyperthermia, indicating that ubiquitination-mediated proteosomal degradation of c-FLIP is not required for its depletion from the cytosol. Here, CFLAR is linked to neoplasm.