Because short-HAVCR1 is associated with rheumatoid arthritis (RA) [49], a Th1- and Th17-mediated disease, and long-HAVCR1 is associated with atopy [60,61], a Th2-mediated disease, our data suggest that the strong cell signaling mediated by short-HAVCR1 skews the immunity towards Th1 and Th17 responses, whereas the weaker long-HAVCR1 signaling favors Th2 responses. This evidence concerns the gene HAVCR1 and rheumatoid arthritis.