In this work, we found that KIN I-derived dermal portions display a variable FGFR2c upregulation, accompanied by a CAF signature (indicated by CSL repression, ULK3 upregulation and the induction of the CAF genes TNC, α-SMA and COX-2) and by a significant increase of autophagic genes and tumor-promoting factors, such as FGF2 and IL-6. The gene discussed is FGF2; the disease is neoplasm.