Summary and conclusions
Understanding the basis of widespread heterogeneity in the manifestations of CRS is advanced by findings that the three main endotypes, T1, T2 and T3, orchestrate the expression of three distinct large sets of genes. It is clear that T2 inflammation can be found around the world and in both CRSwNP and CRSsNP phenotypes. Although the prevalence of T2 endotype in Asia was very low decades ago, it is increasing with industrialization. Another emerging view is that endotype, rather than the phenotype, can drive clinical features, such as the presence of comorbid asthma (T2sNP and T2wNP) and pus (T3sNP and T3wNP). Drugs blocking T2 inflammation can shrink nasal polyps in western countries; as trials are initiated in T2sNP patients, we expect that this very large group of patients will be found to benefit from blockade of type 2 inflammation. Studies of the microbiome may discover that the higher prevalence of T3 forms of CRS in China reflect distinct microbiological exposures. The development and use of improved methods of endotyping disease in the clinic will likely usher in expansion of the use of biological therapies targeting T2 and introduction of treatments targeting other endotypes.