Biffi et al. [8] found that induction of IL-1 by tumor cells stimulates the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway through up-regulation of leukemia inhibitory factor (LIF), leading to the formation of the iCAF phenotype, while tumor-secreted TGF-β inhibits IL-1-induced JAK/STAT signaling, resulting in the suppression of iCAF activation and enhancement of myCAF features. This evidence concerns the gene SOAT1 and neoplasm.