Idiopathic Pulmonary Fibrosis (IPF) is a fatal chronic Interstitial Lung Disease (ILD) affecting mechanical functions and gas exchange, caused by an increased fibroblast activity and collagen deposition that compromise the alveolar-capillary barrier. Identifying an effective therapy for IPF remains a clinical challenge. Chemokines are key proteins for cell communication with biological functions in immunity, tissue homeostasis, or damage, and repair. Chemokine receptor signaling induces lung resident cell activation and proliferation, including alveolar macrophages (AMs) and fibroblasts. AMs are an important chemokine and cytokine source during IPF. Here, we highlight the complexity of this system, and based on insights from genetic and transcriptomic studies, we propose a new role for homeostatic chemokines imbalance in IPF, with implications for putative therapeutic targets.