However, as IL-1β has cell-type-specific effects, thus inducing neutrophilia, leukocytosis, and thrombocytosis in vivo [31,32], it is conceivable that the lack of IL-1RA may enhance IL-1 signaling, which stimulated the proliferation of specific osteoclast precursor subsets. The gene discussed is IL1B; the disease is thrombocytosis disease.