Since the nature of the cell surface molecule that could mediate this phenotype is not known yet, we postulated that contact might be mediated by MHC-I molecules for two reasons: (1) MHC-I molecules are ubiquitously expressed by immune and non-immune cells33 and (2) MHC-I-self-peptide interaction with TCR plays an important role in lymphopenia induced proliferation (LIP) and the subsequent generation of memory cells from naïve CD8 T cells in the absence of cognate antigen34,35. The gene discussed is CD8A; the disease is lymphopenia.