A single genetic lesion affecting JAK/STAT signaling in T-cells is unlikely to result in BIA-ALCL, and in vitro studies suggest that other factors, including IL-2 and IL-6 overexpression, dysregulation of survivin, and aberrantly low levels of the regulatory phosphatase Src homology region 2 domain-containing phosphatase-1, are necessary for BIA-ALCL development [29,41]. The gene discussed is SOAT1; the disease is anaplastic large cell lymphoma.