(Senbanjo and Chellaiah, 2017) Hepatic macrophages, on the other hand, can activate quiescent HSCs via TGF-β and promote survival of myofibroblasts through the secretion of IL-1 and TNF, thereby facilitating fibrosis (Pradere et al., 2013; Fabregat and Caballero-Diaz, 2018) In a study on patients with non-viral HCC, the TME of steatotic HCC subtypes was enriched in immune cells and cancer-associated fibroblasts (CAFs), alongside with an increased CCL2 expression and an over activated TGF-β pathway compared to other HCC subclasses. The gene discussed is TGFB1; the disease is cancer.