For instance, the myeloid C-type lectin-like receptor (MICL/Clec12a) was shown to cross-prime CD8+ T-cells contributing to the development of experimental cerebral malaria [26] and to promote murine viral lymphocytic choriomeningitis virus (LCMV) infections by hampering pathogen clearance [88]. The gene discussed is CLEC12A; the disease is cerebral malaria.