Furthermore, Janus kinase (JAK) inhibitors, such as ruxolitinib, mitigate inflammatory damage by suppressing cytokine production—including IFN-γ, TNF-α, IL-6, and IL-17—through inhibition of JAK1/2 signaling, further expanding the therapeutic landscape for GvHD management [135–137]. The gene discussed is IFNG; the disease is graft versus host disease.