The BIA-ALCL pathogenesis involved in genetic predisposition mainly includes JAK-STAT, DNA methyltransferase 3 alpha (DNMT3A) mutation, Tumor protein p53 (TP53) mutation, programmed cell death 1 ligand 1 (PD-L1) chromosomal copy number aberrations (CNAs), chromosome 20q loss, and carbonic anhydrase 9 (CA9) overexpression. This evidence concerns the gene SOAT1 and anaplastic large cell lymphoma.