The authors found that Atg5+/−/Krasmut cells were resistant to autophagy regulation (induction and inhibition) and displayed mitochondrial dysfunction and increased expression and secretion of protumorigenic cytokines, which led to increased tumour infiltration by M2 macrophages.39 Whether all these properties are due to constitutive activation of autophagy or whether this is due to an Atg5-related effect, however, remains unclear for two reasons: first, the effect on autophagy seems at best moderate in this model; and second, no other autophagy gene was tested. The gene discussed is ATG5; the disease is neoplasm.