It was demonstrated that high levels of DNA damage in blood cancer lines drive nuclear accumulation of ABL1, which in turn phosphorylates YAP on tyrosine 357 [36], a modification that promotes association of YAP with p73 and reduces transcriptional activity of YAP/TEAD complexes [49,50]. Here, YAP1 is linked to hematopoietic and lymphoid system neoplasm.