reported that AKT serine/threonine kinase 2 (AKT2) deficiency led to macrophage polarizing to the M2 phenotype, and AKT2−/− mice exhibited elevated resistance to DSS‐induced colitis, compared to wild‐type mice.[23] Consistent with these findings, immunoblot analysis data demonstrated that γGC treatment effectively inhibited the macrophage polarization to M1 phenotype by repressing the phosphorylation of Phosphoinositide 3‐kinase (PI3K) and AKT2 (Figure 3M,N). The gene discussed is AKT2; the disease is colitis.