Th cells sensitized against autoantigens acquire pathogenicity following two sequential events, namely, activation by their target antigen and a process named “licensing”. Here, we analyzed these processes in a transgenic mouse system in which TCR-transgenic Th-cells specific to hen egg lysozyme (HEL) are adoptively transferred to recipients and induce inflammation in eyes expressing HEL. Our data show that the notion that the lung is the organ where “licensing” for pathogenicity takes place (Odoardi et al., Nature 2012) is based on biased data collected with cells injected intravenously, a route in which most transferred cells enter via the lung. Thus, when activated in vitro and injected intraperitoneally, or are activated in vivo, donor cells migrated simultaneously to the lung, spleen and other tested organs. In all tested organs donor cells undergo “licensing” for pathogenicity, consisting of vigorous increase in number and changes in expression levels of inflammation-related genes, monitored by both flow cytometry and microarray analysis. After reaching their peak numbers, around day 3, the “licensed” donor cells migrate to the circulation and initiate inflammation in the HEL-expressing recipient eyes. Importantly, the kinetics of increase in number and of changes in gene expression by the donor cells were similar in lung, spleen, and other tested organs of the recipient mice. Further, The total numbers of donor cells in the spleen at their peaks were 10–100 times larger in the spleen than in the lung, contradicting the notion of Odoardi et al., that the lung is the organ where “licensing” takes place.