The overexpression of ST6GAL1 in bronchial epithelial cells led to an increased expression of MUC1 and MUC4, while the silencing of ST6GAL1 resulted in a decreased MUC4 expression (144).The highly glycosylated tandem repeat (TR) domain of MUC4 has been hypothesized to impede tumor cell interaction with ECM proteins, suggesting a mechanism by which MUC4 could modulate the physical and biochemical environment of the tumor. This evidence concerns the gene ST6GAL1 and neoplasm.