These data indicate that after overexpressing the N3ICD-activated classical Notch signaling pathway, N3ICD preferentially regulates Hey1 by activating Delta1, but not Hes1. Moreover, to address whether Notch3 regulation of Kibra is specific to epithelial cells, we also tested the expression level of Kibra in the glioma U87 cell line after overexpressing N3ICD. Here, HEY1 is linked to central nervous system cancer.