To the Editor—In response to the statements made by Jacobson et al. [1, 2], our study was not designed to study the utility of an immunological marker (such as antigen-specific CD69 expression) in monitoring the risk of development of cytomegalovirus (CMV) retinitis in human immunodeficiency virus (HIV)–infected patients during highly active antiretroviral therapy (HAART). The study design and primary goal of our investigation was to examine the T cell function profiles in patients with AIDS with CMV retinitis before and after initiating HAART [3]. After we compared these parameters of CMV-specific T cell function, we found that the development of CMV retinitis was associated with poor reactivity of CMV-specific CD4 T cells, and that no evidence of immune rebound in patients with CMV retinitis that developed after initiation of HAART. Furthermore, in our data, no patients with baseline (i.e., before any antiretroviral treatment) frequencies CMV-specific of CD69 expression on CD4 T cells (CD69 cell percentages to CMV on CD4 T cells) >0.5% developed CMV retinitis after starting HAART. However, we did not know if these patients did not receive HAART after baseline assessment or whether the immune parameter could be applied during HAART. Immunity to CMV is complex, and we did not intend to suggest in our article that the percentage of CD4+ T cells expressing CMV-specific CD69 can represent the protective immunity to CMV infection. Actually, the associated poor reactivity of CMV-specific CD4+ T cells may be a result of immune dysregulation rather than deficiency in protective immunity [4, 5]