When comparing scRNA-Seq data of direct lung injury with data of AKI-induced remote lung inflammation relative to respective controls, we found that neutrophils in remote lung inflammation (exclusively intravascular) compared with neutrophils in direct lung inflammation (mostly extravasated) showed much higher innate immune signaling with upregulation of Myd88, a downstream effector of signaling via TLRs in response to damage-associated molecular patterns (DAMPs) (38), and of IL1b, a major effector of early type 1 immune responses (39). The gene discussed is MYD88; the disease is inflammatory response.