As in the case of psoriasis, inhibiting the CD19 expression caused an increase in the concentration of PPARγ, Wnt3a, and β-catenin; therefore, it is probable that CD19 regulates the symptoms of psoriasis and depression through the PPARγ/β-catenin/Wnt3a signaling pathway [25]. This evidence concerns the gene WNT3A and depressive symptom measurement.