They also showed that loss of Klf4 expanded NOTCH1-induced leukemia-initiating cells in mouse T-ALL models, and pharmacological inhibition of JNK using AS602801, JNK-IN-8, and CC401 reduced tumor progression of human T-ALL [99], implying potential collaboration between JNK and NOTCH signaling for strengthening tumor-initiation ability in CSCs. This evidence concerns the gene KLF4 and neoplasm.