Our group is interested in the study of the molecular mechanisms that underlie the regulation of autophagy and their possible role in human disease. The main current focus of the laboratory relates to the characterization of novel autophagic processes that are utilized in unconventional manners by the cells to fulfill atypical biological functions. We have identified a transmembrane protein called TMEM59 that is able to induce a non-canonical autophagic process where the same intracellular, single-membrane vesicles where the protein is located become labeled with LC3 and are more efficiently targeted for lysosomal degradation. This atypical phenomenon is induced through direct engagement of the intermediate autophagic mediator ATG16L1, and seems to be involved in innate immunity against invading microorganisms. Interestingly, there is a coding polymorphic allele of ATG16L1 that increases the risk of suffering intestinal inflammatory diseases as well as other pathologies. We are currently studying the physiological function of TMEM59 using both cellular and animal systems, the molecular mechanisms that this protein utilizes to engage the autophagic machinery in novel, unconventional ways and the implications of these activities and ATG16L1 in human pathology.