We generally believe that under normal conditions, FLCN (RagC and RagD activator) is sequestered outside the lysosomal membrane by Rag‐Ragulator complex, and loss of function FLCN mutation leads to Birt‐Hogg‐Dubé syndrome, a disorder characterized by benign skin tumors.[2] We then hypothesis that FLCN is sequestered by the Gal3‐CaN‐Smurf1 complex in order to keep it away from the Rag‐Ragulator complex, preventing FLCN from exerting its GAP enzyme activity for RagC and RagD activation. This evidence concerns the gene LGALS3 and benign neoplasm of skin.