For example, 1) heterozygous deletion of Becn1 increases the formation of malignancies in mice [47]; 2) BECN1 phosphorylation by AKT1 contributes to fibroblast transformation [48]; 3) increased levels of BECN1 compromise breast xenograft formation in vivo [49]; and 4) knock-in mice harboring a BECN1 mutation that prevents binding with its inhibitor BCL2 inhibit HER2+ tumor formation [34]. The gene discussed is BCL2; the disease is neoplasm.