SP110 acts offensively as a leukocyte expression that mediates SP110 with macrophages to downregulate inflammation gene expression via altered TLR4 activity or STAT1 mediation during myeloid differentiation; therefore, mutations in immune SP110 are associated with immunodeficiency syndromes, and SP140 acts as a chromatin reader that enhances STAT1/IRF1 activity and promotes immune checkpoint evasion. This evidence concerns the gene STAT1 and immunodeficiency disease.