Some scholars have investigated this issue, and data suggest that IL-2 inducible T-cell kinase (ITK) is crucial in the differentiation of T helper cell subpopulations, ITK activation is up-regulated in patients with RA, and ITK inhibitors alleviate arthritic inflammation by regulating the Foxo1 translocation, inhibiting the phosphorylation of PLC-γ1, an important mediator of the ITK signalling pathway, and rebalancing Th17 and Treg cells. The gene discussed is ITK; the disease is rheumatoid arthritis.