Next, to determine the functional consequences of these Cre-mediated cell-specific Myd88 deletions, we incubated whole blood leukocytes, alveolar and peritoneal macrophages and splenocytes obtained from LysM-Myd88−/−, Tie2-Myd88−/− and control mice with K. pneumoniae LPS or heat-killed K. pneumoniae, using TNFα release as readout; we focused on these cell types since they confer protective functions during infection and sepsis [24]–[26]. The gene discussed is TEK; the disease is infection.