Intriguingly, although well known for its ability to sequester and inactivate the tumor suppressor TP53, mortalin depletion induced p21CIP1 transcription in TP53-deficient BRAF tumor cells, for which activation of the transcription factor Sp1 by upregulated Raf/MEK/ERK activity was necessary [98]. The gene discussed is TP53; the disease is neoplasm.