MYD88 and neoplasm: For instance, the binding of Fusobacterium to E-cadherin resulted in pro-inflammatory responses.8 In HCT116 colorectal cancer cells, F. nucleatum promoted the upregulation of TLR4 and MyD88 and the activation of the major immunological transcription factor NF-κB.13 Such inflammatory responses were not limited to in vitro models, as F. nucleatum induced a pro-inflammatory environment in tumor tissue in infected Apcmin/+ mice.3 Similarly, the presence of F. nucleatum correlated with a pro-inflammatory tumor microenvironment in human CRC tissue from the Cancer Genome Atlas (TCGA).3