A mechanistic study revealed that the 30–466 nt region of AK085865 specifically binds to interleukin enhancer-binding factor 2 (ILF2) and plays a negative regulatory role in the miR-192 pathway mediated by the ILF2-ILF3 complex, thereby promoting the polarization of M2 macrophages and reducing the symptoms of myocarditis [72]. Here, ILF2 is linked to myocarditis.