Although in contrast with what was described above, this regulatory mechanism, if confirmed with additional mechanistic insights and in other experimental settings, would at least partially explain a couple of observed biological events: the high turnover of TAZ (compared to the stability of YAP and considered the “double” regulation of the protein by ubiquitin on the additional phosphodegron at the N-terminus not shared by YAP) and the tumor suppressor properties of YAP [27,28]. This evidence concerns the gene WWTR1 and neoplasm.