Thus, combined gefitinib-DAPT treatment of Balb/c nu/nu mice with EGFR-TKI acquired resistant NSCLC xenografts resulted in marked tumor growth retardation, decreased proliferative activity, and increased apoptotic cell death accompanied by upregulation of active Caspase-3 and EMT phenotype attenuation [134], while co-administration of BMS-708163 and gefitinib resulted in marked reduction of tumor size, increased levels of Caspase-3, and decreased expression of Ki-67 [136]. Here, MKI67 is linked to neoplasm.