Application of tofacitinib, a drug approved for treatment of RA and inflammatory bowel disease (IBD), on TNF-α/IL-17A–triggered BMS astrocyte/NGN2-neuron cocultures resulted in the loss of BMS astrocytes’ ability to protect neurons against the TNF-α/IL-17A–induced neurite damage. The gene discussed is IL17A; the disease is inflammatory bowel disease.