Current models of SS pathogenesis—developed from limited laboratory studies of serum and skin inflammatory mediators and case reports of targeted therapeutic trials—are incomplete but suggest that infection, cancer, and drug reactions drive heightened levels of TNFα, IL-1, and G-CSF that promote leukocytosis.3 In the context of hematologic cancer, aberrant malignant neutrophils further contribute to leukocytosis following treatment with G-CSF, all-trans retinoic acid, or FL3 inhibitor. The gene discussed is CSF3; the disease is hematopoietic and lymphoid cell neoplasm.