We expected that knockdown of calreticulin would prevent normal APM functions and thus impair T-cell recognition of tumor [22]; that silencing of PERK would maintain APM functions but prevent calreticulin translocation [3, 17]; and that peptide blocking would prevent surface calreticulin/T-cell interactions, whereas the presence of exogenous calreticulin would promote those interactions. The gene discussed is CALR; the disease is neoplasm.