In addition, in characteristic dermatitis (AD) studies, UV-treated riboflavin was found to inhibit the activation of NLRP3 inflammatory vesicles in macrophages by inhibiting the H3K9 lactation of NLRP3 and ASC, leading to a reduction in IL-1β secretion and M1 macrophage polarization, as well as a reduction in TSLP secretion by keratin-forming cells to attenuate AD progression (148). This evidence concerns the gene NLRP3 and skin disorder.