Other genes affected by therapeutic blocking of miR-142-5p as listed in S1 and S2 Tables that could also interfere with cross-talk interactions that NF-κB is a part of, are Nr5a2,[43] Cftr,[44] TNFRSF11b,[45] Adora1 (adenosine A1 receptor)[46] and PLAT.[47] In conclusion, in our model of blocking miR-142-5p in transfer-colitic mice, it is possible that systemic effects of the treatment are responsible for maintaining a healthy body weight, possibly by preventing immune-mediated cachexia. The gene discussed is CFTR; the disease is Cachexia.