DCs from HCC patients have an impaired ability to trigger immune response, in the meantime of promoting immunosuppression.103 Modulating the lipid metabolism, such as de novo FAS during DCs activation, affects endoplasmic reticulum (ER) and Golgi expansion, thereby impacting their antigen‐presenting ability.104 In a setting of HCC, the tumour‐associated dendritic cells (TADCs) express the scavenging receptor, such as macrophage scavenger receptor 1(MSR1) that facilitates lipid uptake and accumulation, which seems to support the immunogenic immune responses and cross‐presentation. This evidence concerns the gene FAS and neoplasm.