This finding was supported by Li et al., who simulated an airway infection in a mouse model of steroid-resistant asthma through the concomitant administration of LPS + IFNγ; consequently, PP2A activity (that induced JNK) was attenuated and led to the phosphorylation of GR-α at Ser226, thereby hindering glucocorticoid receptor nuclear translocation in pulmonary macrophages [66]. Here, NR3C1 is linked to asthma.