MT1A and intestinal neoplasm: Similar evidence in support of this idea has been seen in intestinal tumor models, wherein intestinal epithelial cell-specific TBK1 knockdown increased the expression of the pro-inflammatory immune regulator, metallothionein 1 (MT1), leading to the expression of IL1β in macrophages and differentiation of pro-inflammatory Th17 cells, resulting in inflammation and colorectal tumorigenesis [52].