Alternatively, when LATS1/2 are inactivated due to the upregulation of DCLK1, the nuclear translocation of cytoplasmic YAP1 is increased, and the expression of target genes involved in CSC traits, such as self-renewal, proliferation and tumor growth, is consequently increased via interactions of YAP1 with TEADs and TAZ. The gene discussed is LATS1; the disease is neoplasm.