IRAK1 is a serine/threonine protein kinase that functions as a critical initiator of innate immune responses through toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) signaling 1. Upon TLR activation, IRAK1 is rapidly recruited by MYD88 adaptor protein, phosphorylated by IRAK4, and undergoes autophosphorylation to become catalytically active 2. Activated IRAK1 phosphorylates downstream targets including E3 ubiquitin ligases and interferon regulatory factor 7 (IRF7), culminating in NF-κB nuclear translocation and type I interferon production to establish antiviral immunity 3. In hematologic malignancies, IRAK1 acts as an oncogenic dependency: gain-of-function MYD88 mutations in diffuse large B-cell lymphoma (DLBCL) spontaneously activate IRAK1/IRAK4 signaling, promoting survival through sustained NF-κB and JAK-STAT3 activation 1. In glioma, radiation-induced IRAK1 expression mediates radioresistance by stabilizing the antioxidant enzyme PRDX1 and suppressing autophagic cell death 4. IRAK1 gene polymorphisms associate with inflammatory arthritis and ankylosing spondylitis susceptibility 56. These findings establish IRAK1 as both a fundamental innate immune signaling hub and an emerging therapeutic target in malignancy and inflammation 7.