To understand if epithelial CAMP or DEFB4 secretion was helping to control bacterial burden by enhancing autophagy in macrophages, even if CAMP was undetected in the media supernatant in control experiments, we probed for colocalization of Mtb and LC3 protein, a marker of autophagosomes, in (1,25D-treated) infected macrophages 3 days after infection. The gene discussed is MAP1LC3A; the disease is infection.