ITGAM encodes the alpha-M subunit of integrin Mac-1 (CD11b/CD18), a key adhesion molecule on myeloid cells including monocytes, macrophages, and granulocytes. The protein functions as complement receptor type 3 (CR3), binding iC3b fragments and recognizing fibrinogen and factor X, thereby mediating uptake of complement-coated pathogens and facilitating cell–cell adhesion through interactions with ICAM-1 on endothelial cells. ITGAM also regulates neutrophil migration and, in association with ITGB2, is required for CD177-PRTN3-mediated neutrophil activation. ITGAM polymorphisms are strongly associated with systemic lupus erythematosus (SLE) across multiple ethnic populations, with certain alleles conferring elevated disease risk 1. The gene has been identified as a plausible therapeutic target in lupus nephritis 2. Recent evidence suggests CD11b agonists, such as GB1275, can enhance anti-tumor immunity by reprogramming tumor-associated macrophages through STING-interferon signaling activation and NF-κB repression, with efficacy demonstrated in phase I human trials 3. Additionally, ITGAM polymorphisms associate with IgA nephropathy susceptibility in Chinese Han populations, with protective alleles correlating with preserved renal function 4. In triple-negative breast cancer, CD11b-mediated neutrophil adhesion to tumor cells promotes cancer progression via MAPK pathway activation, and blocking this interaction with atorvastatin inhibits tumor cell invasion 5.