(155) explored such interaction on samples derived from allergic asthma patients, evidencing an increased expression of natural cytotoxic receptors NKp30 and NKp46 on iNKT cells from patients with allergic asthma, as well as an elevated secretion of granzyme B and perforin by these cells, which led to an increased cytotoxicity of iNKT cells against autologous Treg cells, suggesting that the reduction of Treg cells caused by iNKT cells could be mediated either by the direct interaction or through the secretion of the aforementioned cytotoxic enzymes. The gene discussed is NCR1; the disease is allergic asthma.