Following this switch, KANK1 competes with SCRIB for NOS1AP binding, which in turn compromises SCRIB-mediated Hippo signaling leading to significantly decreased phosphorylation of TAZ, increased stabilization of TAZ and elevated nuclear accumulation of TAZ followed by promoting the tumor-initiating potential of breast cancer stem cells as well as the transcription of growth promoting and cell survival genes (Fig. 10e). The gene discussed is KANK1; the disease is neoplasm.