M. pneumoniae can induce mucin overproduction by inhibiting the transcription suppressor FOXA2 Lung function is improved by restoring FOXA2’s transcription suppressor function and downregulating goblet cell hyperplasia and metaplasia (GCHM)-promoting pathways in M. pneumoniae-infected airways in asthma patients with abnormal mucin secretion and accumulation in airway lumens, which are clinical markers of asthma (Hao et al., 2014). This evidence concerns the gene FOXA2 and asthma.