Overall, our data appear to suggest the possibility that the upregulation of FGFR2c in KIN I fibroblasts could contribute not only to a CSL/ULK3-dependent precocious CAF and autophagic signature but also to an effective enhancement of autophagic membrane trafficking, which possibly might underly the increased release of tumor-promoting factors, such as IL-6. This evidence concerns the gene ULK3 and neoplasm.