In a study of HF in mice treated with carbon tetrachloride, TGF-β1 induced FAK activation in a time-and dose-dependent manner, and FAK activation was associated with increased expression of α-SMA and collagens in fibrotic liver tissue, while inhibition of FAK activation (Y397 phosphorylation of FAK) with FAK inhibitors (PF 562271) blocked α-SMA and collagen expression in TGF-β1-treated HSCs and induced apoptotic signaling, inhibiting the formation of stress fibers, thereby attenuating HF in mice (Xing et al., 2021). This evidence concerns the gene TGFB1 and hydrops fetalis.