Phosphorylated STAT3 translocates from cytoplasm to the nucleus, where it binds promoter regions to initiate target gene transcription.[49] It is worth noting that the activation of STAT3 in the transcriptional regulation of Cxcl1 has been implicated in the mechanisms of tumor diseases and immune disorders,[23, 24] supporting our hypothesis that RIPK1 promotes Cxcl1 expression via JAK1‐STAT3 signaling in AECs in response to inflammatory stimulation. Here, CXCL1 is linked to neoplasm.