Indeed, preliminary studies have as yet shown that rhIL-15 and IL-15 superagonists can reduce skin inflammation in lesional human psoriasis skin [35] and in an IL-15−/− mouse model of “atopic dermatitis.” [34] Incidentally, our pilot study also introduces IFNγ as an apoptosis-inducing cytokine in native dermal CD68+ and CD206+ MACs in human skin, which may contribute to the perpetuation of chronic skin inflammation by reducing the pool of immunoinhibitory dermal MACs. This evidence concerns the gene CD68 and psoriasis.