ASCL1 and neoplasm: In line with this, KDM5A promoted SCLC proliferation by repressing Notch2 and Notch signaling and sustaining expression of a neuroendocrine TF ASCL1, while KDM5A knockout restored expression of Notch2 and Notch target genes, reverting ASCL1 expression and blocking tumor growth and thus suggesting KDM5A as a possible therapeutic target in SCLC [287].