Interestingly, increased levels of TNF-α, MIG, and KC have been observed in models of highly pathogenic influenza infection [26], [51], [52], suggesting that failure to properly regulate expression of NKG2A on effector cells may contribute in part to enhanced expression of pro-inflammatory mediators and exacerbated pulmonary pathology during highly pathogenic influenza infection. The gene discussed is KLRC1; the disease is influenza.