Given the overexpression of LPAR1 in human HCC and the ability of LPAR1 depletion to induce oncogene-induced senescence (Fig. 1), we sought to analyze whether inhibition of the LPAR1–Filamin A interaction is sufficient for senescence induction, reorganization of the actin cytoskeleton and focal adhesions. The gene discussed is FLNA; the disease is hepatocellular carcinoma.