Given the loss of autophagy in APC leads to increased secretion of IL-1 family cytokines and IL-23 upon inflammatory stimulation, it is perhaps not surprising that mice with autophagy-deficient myeloid cells (Atg5fl/fl-LysM Cre mice) show elevated serum IL-17 in response to infection with Mycobacterium tuberculosis (60). The gene discussed is IL1A; the disease is infection.