ECD is a multifunctional regulator of p53 stability and cell cycle progression. It inhibits MDM2-mediated degradation of p53, possibly through cooperation with TXNIP, and has intrinsic transactivation activity enhanced by EP300. ECD regulates transcription of glycolytic genes and may disrupt Rb-E2F binding to promote E2F-dependent transcription. Its cell-cycle function depends on RUVBL1-mediated association with the R2TP complex. ECD also participates in pre-mRNA splicing and, together with DDX39A, in mRNA nuclear export. In cancer biology, ECD functions as an androgen receptor target gene that promotes prostate cancer tumorigenesis by regulating glycolysis 1. In prostate cancer tissues, ECD is overexpressed and its overexpression predicts shorter survival. ECD associates with mRNA of key glycolytic genes and maintains their stability, driving increased glucose uptake and glycolytic flux in cancer cells 1. Enzalutamide treatment, an AR antagonist, decreases ECD levels, and ECD knockout reduces oncogenic traits in prostate cancer cell lines 1. These findings position ECD as a potential therapeutic target in AR-driven malignancies, though clinical development remains preliminary.