Another study by the Tuveson laboratory characterized different CAF subtypes by revealing that TGFβ/SMAD2/3 signaling is key in activating myCAFs near tumor cells where the TGFβ gradient is high and that IL1α/JAK/STAT signaling is essential for activating iCAFs in regions where the TGFβ gradient diminishes, illustrating how spatial variations in the TGFβ concentration influence CAF phenotypic differentiation53. The gene discussed is TGFB1; the disease is neoplasm.