The same authors also demonstrate that stable silencing of ATG5 or ATG7 enhances apoptosis and inhibits luminal colonization in a 3D culture model of MCF-10A breast cancer cells.24 Autophagy activation is also a general mechanism that cancer cells use to overcome the potential stress induced by hyper-activated tyrosine kinases in the absence of their key adaptor proteins tethering partners.25, 26 Sandilans and colleagues show that perturbations of the Integrin signaling through the FAK/Src axis, lead to the selective targeting of hyper-activated Src to autophagy degradation. The gene discussed is ATG5; the disease is cancer.