Our results associate keloid tissues with an inflammatory milieu representing multiple T-helper pathways, including the Th2 (e.g. IL-4R, CCL11, TSLP, TNFSF4/OX40L, TNFRSF4/OX40), Th1 (e.g. IFNγ, CXCL10/11), Th17/Th22 (e.g. PI3, CCL20, S100As) axes, as well as the JAK/STAT signaling molecule JAK3. Here, SOAT1 is linked to keloid.