The results showed for the first time that severe type 2 inflammation induced high levels of PAF-associated pathophysiology and that the main cause of the high PAF-associated pathophysiology appears to derive from high lyso-PAF and PAF synthesis via overexpressed LPCAT1 and LPCAT2 compared to the cluster of moderate-to-low type 2 inflammatory types of CRSwNP (cluster 1) (Figure 6). The gene discussed is LPCAT1; the disease is chronic rhinosinusitis with nasal polyps.