Angiogenic stimulators promoted endothelial cell proliferation and resulted in uncontrolled growth.[7] A recurrent t (1;3) (p36.3; q25) chromosomal translocation, YAP1-TFE3 fusion, and WWTR1-CAMTA1 rearrangements in EHE patients drive the tumor biology, and a recent study showed that interaction of the ATAC complex with YAP1-TFE3 and WWTR1-CAMTA1 fusion plays a pivot role in the oncogenicity.[8,9] It indicates a unifying enzymatic therapy target for EHE. This evidence concerns the gene XCL1 and neoplasm.