Furthermore, our data showed that tmTNF-α exerted beneficial effects via TNFR2 through activation of the AKT pathway, a cardioprotective signaling pathway [32–35], and inhibition of the NF-κB pathway, which is involved in cardiac hypertrophy, adverse remodeling, and inflammation [36–38]. The gene discussed is NFKB1; the disease is cardiac hypertrophy.