When transferred into tumor-bearing mice, high-avidity CTLs were shown to be more potent than low avidity CTLs to infiltrate tumors (174, 175, 177), which could be partly attributed to the expression of integrins and lectins, such as CD62L and CD11a, on high avidity CTLs (174), and the recognition of tumor antigens (32), emphasizing the role of antigen as homing molecule. The gene discussed is ITGAL; the disease is neoplasm.