Intestinal epithelia express two myosin light chain kinase (MLCK) splice variants (the full‐length and shorter isoform MLCK2). In IBD patients, the pro‐inflammatory cytokine tumour necrosis factor (TNF)‐like 1A (TL1A) was demonstrated to activate the phosphatidylinositol 3‐kinase/protein kinase B (AKT) signals and up‐regulate the MLCK splice variant (MLCK2), which might induce the MLCK‐mediated terminal web contraction, and invoke bacterial internalisation (Figure 2A).39 This evidence concerns the gene AKT1 and inflammatory bowel disease.