In rare tumors, the oncogenic activation of TAZ and YAP can occur as a consequence of chromosomal alterations that generate gene fusions, leading to the expression of chimeric proteins such as TAZ-CAMTA1 and YAP-TFE3 that drive epithelioid hemangioendothelioma (EHE) in humans and mouse models [65,66,67,68]. This evidence concerns the gene YAP1 and epithelioid hemangioendothelioma.