For example, it triggers the generation of free radicals like reactive oxygen/nitrogen species (ROS/RNS) (7) and activation of key intrinsic factors like NFkB and STAT-3, which in concert with proliferation-induced mutagenesis not only fosters the tumor-promoting inflammatory microenvironment but also orchestrates stimulation of distinct neoplastic programs leading to subsequent progression of HCC (8). The gene discussed is STAT3; the disease is neoplasm.