Importantly, the disease-promoting effects of MyD88 in the model of intranasal BLM administration seemed to be independent of TLR2/4 signaling but rather linked to the function of MyD88 in IL1R1 signaling since IL1R−/− but not TLR2−/−/TLR4−/− mice were also protected from BLM-induced fibrosis in this model [171]. This evidence concerns the gene TLR2 and Bloom syndrome.