The binding interface of the Beclin-1 homodimer was modelled by Yang et al., followed by the selection of a 15-residue fragment in the binding interface, which allowed the design of a stapled peptide that induced autophagy, contributing to the death of EGFR/HER2-driven cancer cells and exerting potent antiproliferative effects [175,176]. This evidence concerns the gene BECN1 and cancer.