In this context, our observation that glutamate stimulation of keloid fibroblasts markedly induced CXCL2, CXCL3, and CXCL8 suggests that glutamine–glutamate metabolic reprogramming may reinforce a chemokine-driven inflammatory circuit that sustains leukocyte recruitment and fibroblast activation within keloid lesions. The gene discussed is CXCL3; the disease is keloid.