We argue that Cav1 expression may be linked to IP collapse via upregulation of defined molecules that have previously been shown to act as guardians of HF IP (CD200, IL-10, α-MSH, IGF1, TGF-β2), or via downregulation of molecules associated with HF-IP collapse (substance P, MHC class I/II, ß2-microglobulin, IFN-y, CXCL-9, -10, -11, CXCR3 and CD123), or the promotion of EMT in bulge epithelial stem cells (TWIST1, SNAIL, SLUG, vimentin, fibronectin, N-cadherin) [7,8,73,75]. The gene discussed is SNAI2; the disease is hydrops fetalis.