The inhibition of HDACs can relieve this repression and upregulate miR-15 and let-7, downregulating BCL2 expression level and promoting tumor apoptosis.28 Selective inhibition of HDAC3 restores immunosurveillance in CREBBP-mutant DLBCL.29 Moreover, HDACi can downregulate the expression levels of MYC, BCL2, and BCL-x genes by inhibiting the HDAC/STAT3/Bcl-2 and JAK2/STAT3 signaling pathways, promoting the apoptosis of cancer cells.30,31 Thus, HDACi can be potential therapeutic drugs for DEL. The gene discussed is STAT3; the disease is neoplasm.