Considering the previous reports describing the tumor suppressive roles of DKK3 [13,15,19,20], its inhibitory effect on malignant TGF-β signaling [20,24], and its potential in recent clinical trials [21,22], we have focused on reactivating endogenous DKK3 expression using a CRISPR-based approach. The gene discussed is TGFB1; the disease is neoplasm.