Additionally, emerging studies have proposed that neuroinflammation and the proinflammatory cytokine interleukin 6 (IL‐6), which are crucial pathological hallmarks of AD, could potentially inhibit TET3 expression in a Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3)‐dependent manner, leading to the downregulation of Neurogenic differentiation 1 in neural stem cells [102]. The gene discussed is STAT3; the disease is Alzheimer disease.