The article investigates the role of myeloid inhibitory C-type lectin-like (MICL) in regulating neutrophil extracellular trap (NET) formation and its implications in disease. MICL is an inhibitory C-type lectin receptor that directly recognizes DNA in NETs, playing a crucial role in controlling neutrophil activation and NET formation. Loss or inhibition of MICL leads to uncontrolled NET formation through the ROS–PAD4 pathway, resulting in an auto-inflammatory feedback loop. This dysregulation exacerbates pathology in rheumatoid arthritis, both in mouse models and human patients, where autoantibodies to MICL inhibit its key functions. Anti-MICL autoantibodies are also detected in patients with other diseases linked to aberrant NET formation, such as lupus and severe COVID-19. However, in the context of fungal infections, such as Aspergillus fumigatus, dysregulation of NET release by MICL is protective. The study highlights that the recognition of NETs by MICL is a fundamental autoregulatory pathway that controls neutrophil activity and NET formation, with implications for both inflammatory and infectious diseases.The article investigates the role of myeloid inhibitory C-type lectin-like (MICL) in regulating neutrophil extracellular trap (NET) formation and its implications in disease. MICL is an inhibitory C-type lectin receptor that directly recognizes DNA in NETs, playing a crucial role in controlling neutrophil activation and NET formation. Loss or inhibition of MICL leads to uncontrolled NET formation through the ROS–PAD4 pathway, resulting in an auto-inflammatory feedback loop. This dysregulation exacerbates pathology in rheumatoid arthritis, both in mouse models and human patients, where autoantibodies to MICL inhibit its key functions. Anti-MICL autoantibodies are also detected in patients with other diseases linked to aberrant NET formation, such as lupus and severe COVID-19. However, in the context of fungal infections, such as Aspergillus fumigatus, dysregulation of NET release by MICL is protective. The study highlights that the recognition of NETs by MICL is a fundamental autoregulatory pathway that controls neutrophil activity and NET formation, with implications for both inflammatory and infectious diseases.