Furthermore, c-aAb targeting IFNγ, interleukin (IL)-6, and granulocyte-macrophage colony-stimulating factor (GM-CSF) have been associated with increased susceptibility to various infections in humans such as non-tuberculosis mycobacteria, Staphylococcus aureus, and aspergillus (6, 16–18), and GM-CSF c-aAb are counted as a diagnostic factor for pulmonary alveolar proteinosis (PAP) (19). Here, CSF2 is linked to tuberculosis.