DAPK-1- and TGFβ-driven autophagy, therefore, can be viewed as dual-modelparadigms in which autophagy may contribute to tumor suppression early in the development of asubset of HER2 gene-amplified breast carcinomas; however, when these tumors somehow bypass the tumorsuppressor activity of DAPK-1 and TGFβ, autophagy would later allow the selection ofinvasive, mesenchymal cells with an enhanced expression of autophagic and stem cell markers. Here, ERBB2 is linked to breast carcinoma.