In P2, the massive smooth muscle infiltration by clonal expansion of CD8+ T cells expressing granzyme B and IFN-γ led us to select the JAK1/2 inhibitor ruxolitinib, which we had previously used successfully to treat autoimmune enteropathy induced by STAT3 GOF [5, 11], with the goal in mind to block signals from cytokines such as IL-2, IL-15 that are central for CD8+ T-cell activation, and IFN-γ that mediates some of CD8+ T-cell deleterious effects. The gene discussed is IL2; the disease is autoimmune enteropathy.