Nonetheless, the expression of inhibitory immune checkpoints, such as LAIR1, and their engagement with CI activate the receptor that is intimately tied to the downstream signaling of immunoreceptor tyrosine-based inhibitory motifs and the recruitment of SHIP1–2 and Src2 domain-containing phosphatase-1, therefore leading to negative regulatory effects on immune cells, as demonstrated in many inflammatory contexts, including rheumatoid arthritis, systemic lupus erythematosus, and recently in allergic asthma [34,35]. The gene discussed is LAIR1; the disease is systemic lupus erythematosus.