Our co-immunoprecipitation assays revealed that the increase of autophagosome formation in MCF-7TR5 cells may be due to the dissociation of Bcl-2 from Beclin 1, which further results in the enhancement of interaction among the ATG14-Beclin1-PI3KC3 complex, suggesting that the alteration of Bcl-2 and Beclin 1 interaction may, at least in part, responsible for the activation of pro-survival autophagy in TAM-resistant breast cancer cells. The gene discussed is BCL2; the disease is breast cancer.