As treatment with TCA is known to elongate the bile canaliculi network [33], and drug-induced cholestasis is strongly associated with deformation of the bile canaliculi [23], we investigated bile canaliculi dynamics via S1PR2 in HepG2-NIAS cells using TCA, both predominant BSEP substrate and S1PR2 ligand [24], and S1P2 agonist. This evidence concerns the gene S1PR2 and cholestasis.