JAK2 and silicosis: In our study, significant BIC-induced inhibition of the phosphorylation levels of both JAK2 and STAT3 was observed in lung tissues of the silicosis rat model and macrophages in vitro, leading to down-regulation of SOCS3 in a cascade of diminished secretion of inflammatory cytokines, such as TNF-α, IL-1β, and IL-6 [32, 33], as well as negative feedback regulation of JAK2 phosphorylation [31].