It is further noteworthy that while the mechanism of weak TCR signal failing to curtail STAT5b activity has not yet been studied in the human TCR signaling defects, gain-of-function missense mutations in STAT5b, and JAK1—which activates STAT5b—are associated with syndromes characterized by profound early onset dermatitis and eosinophilia (75, 76). The gene discussed is STAT5B; the disease is dermatitis.