In mouse syngeneic or xenograft models that were treated for oncogene inhibition (anti-Her2 and anti-ER treatments), primary tumors regressed leaving residual tumor cells locally or at remote sites, that exhibited reduced proliferation and a gene signature with reduced expression of Cyclins and CDKs, enhanced expression of ECM proteins (e.g., Fibronectin) and dormancy genes, such as Bhlhe41 (coding for DEC2), TGFβ2 and its receptor TGFβRIII, and Thsb1 (coding for Tsp-1). Here, BHLHE41 is linked to neoplasm.