suggested that the 9p24.1 alterations represented a common mechanism of PD-L1 overexpression in the BIA-ALCL, possibly acting synergistically with constitutive pSTAT3 signaling, while PD-L1 expression might be induced by JAK/STAT signaling alone and/or other alternative pathways in PD-L1-positive cases without chromosomal aberration (37). This evidence concerns the gene SOAT1 and anaplastic large cell lymphoma.