Stationary HSCs mainly maintain liver homeostasis and prevent HCC development, while activated myofibroblast HSCs (myHSC) promote tumor cell proliferation and malignant transformation.[6] The balance between different HSC subtypes, such as cytokine‐ and growth factor‐expressing HSCs (cyHSCs) and myHSCs, may be critical in determining the pro‐ or anti‐tumorigenic effects of the HCC microenvironment.[6] Our study revealed a significant upregulation of miR‐500a‐3p expression in HCC tissues compared to normal liver tissues, with predominant overexpression in α‐SMA+ myofibroblast regions. The gene discussed is ACTA1; the disease is neoplasm.