This largely depends on Hippo-YAP signaling in a non-cell-autonomous manner.276 On the basis of such a dependency, coupled with the well-recognized cell-autonomous role of YAP1 and the involvement of CXCL5 in EMT,250,274,277 it is reasonable to hypothesize that a subpopulation of cancer cells characterized by a mesenchymal signature may be localized at invasive fronts, which would facilitate the establishment of an immunosuppressive TME through selective secretion of chemoattractants like CXCL5, thus resulting in resistance and metastasis. The gene discussed is CXCL5; the disease is cancer.