The abrogation of DLL4 expression in LFS is a novel discovery, which to our knowledge has never been reported before, especially in light of the fact that the main characteristic feature of LFS has always been the germline and autosomal dominant heterozygous mutation of TP53. However, a similar down-regulation of DLL4 both at the transcriptional and translational levels in other cancer lines and tumor tissues was unexpected and antithetical to published reports that emphasize DLL4 as a tumor promoter and an aberrant activator of the Notch receptor. The gene discussed is TP53; the disease is neoplasm.