Figure 4: Mechanistic diagram that shows MUC1’s anti-inflammatory properties. MUC1 is known to inhibit several toll-like receptors (TLR) through MyD88 recruitment. This results in preventing various downstream signaling cascades, such as c-Jun N-terminal kinase (JNK), p38 mitogen activated map kinase (p38MAPK) and extracellular signal-regulated kinase (ERK1/2), which would lead to the transcription of different pro-inflammatory genes. Dexamethasone (DEX), among other corticosteroids, is known to increase the expression of membrane-tethered MUC1 which would result in increasing its anti-inflammatory capacity. However, corticosteroid receptor (GR) modifications, such as an increased GRα phosphorylation (P) at Ser226, mediated by JNK, p38MAPK and ERK1/2, contributes to steroid resistance by preventing nuclear translocation, thus could have an effect in MUC1 expression. Additionally, the possibility of a potential interaction between MUC1 cytoplasmic tail (MUC1-CT), corticosteroids and their receptors is currently unknown.