Adding to the therapeutic potential of manipulating JAK-STAT signaling, a study by Borbély et al. (2022) found that inhibitors targeting this pathway ameliorated stress-induced reductions in adult neurogenesis and alleviated associated anxious-depressive behavior in murine models, leading to the initiation of a Phase I/II clinical trial aimed at assessing these inhibitors in human patients diagnosed with treatment-resistant depression [264]. This evidence concerns the gene SOAT1 and depressive disorder.