RTN4 and hepatocellular carcinoma: Knowing that YAP/TAZ is involved in lipid metabolic reprogramming, it is plausible that its hyperactivation, triggered by heightened Nogo-B signaling, leads to excessive accumulation and release of FA through increased activation of SREBP1, which may furnish HCC cells with an ample energy source, thereby promoting HCC progression and fostering the creation of an immunosuppressive TME, ultimately driving the polarization of TAM toward an M2 phenotype.