The mechanisms involve both the tumor’s own pathological effects—such as secreting inflammatory cytokines like IL-6 and TNF-α, which synergize with T2DM-induced insulin resistance to exacerbate hepatic oxidative stress, and space-occupying effects that directly impair hepatic blood flow or trigger “aseptic hepatitis”—and the multi-target hepatotoxicity of anticancer drugs. This evidence concerns the gene IL6 and neoplasm.