To test the hypothesis that Atg9a activity conferred susceptibility to Bm16M infection, we examined Bm16M replication in Atg9a−/− MEF cells (Saitoh et al., 2009; Figure 5A), as well as in RAW264.7 macrophages depleted of the protein via lentiviral mediated gene silencing (Figure 5B). The gene discussed is ATG9A; the disease is infection.