-Corticosteroid receptor isoforms:
     - Decreased corticosteroid receptor α isoform.
     - Increased corticosteroid receptor β isoform.
     - Imbalance of the ratio between these two corticosteroid receptor isoforms.
-Increased expression of pro
     - inflammatory transcription factors, such as:
     - Nuclear factor kappa beta (NF-kβ)
     - Activator protein-1 (AP-1)
-Corticosteroid receptor modifications: Increased phosphorylation of residues decreases nuclear translocation capacity.
GRα phosphorylation at Ser226 contributes to steroid resistance by preventing nuclear traslocation. This residue has been described to be phosphorylated by:
     - Activation of p38 mitogen activated map kinase (p38MAPK).
     - Increase in extracellular signal- regulated kinase (ERK).
     - Increase in c-Jun N-terminal kinase (JNK)
     - Decrease in MKP1.
-Defect in histone acetylation.
Table 2: Corticosteroid resistance molecular mechanisms in chronic rhinosinusitis with nasal polyposis (CRSwNP). Similarities with asthma [41].