TET2 (the primary CHIP gene) and other CHIP genes (e.g., DNMT3A, EZF2) act as epigenetic mediators, increasing the likelihood that molecular mechanisms associated with gout involve training phenomena, where external stimuli (in this case, soluble urate) reprogram the epigenome to train the innate immune system to exhibit a heightened response to MSU crystals (Joosten et al., 2020). The gene discussed is DNMT3A; the disease is gout.