Extending these findings, a recent study found that deletion of the protocadherin Fat1 in a mouse model of cSCC promoted a hybrid EMT phenotype by inducing YAP nuclear translocation and ZEB1 expression that stimulates the mesenchymal state, while increased expression of the cancer SC factor SOX2170 sustains the epithelial state35 (Figure 3). The gene discussed is YAP1; the disease is cancer.