This review synthesizes the canonical and non-canonical functions of AARS1/2, with a particular focus on their lactylation-related mechanisms; details how lactylation acts as a mechanistic bridge linking AARS1/2 to diverse oncogenic signaling pathways, thereby promoting cancer hallmarks such as metabolic reprogramming, uncontrolled proliferation, immune escape, and therapy resistance; and proposes strategies to target AARS1/2 or modulate relative lactylation, offering a potential avenue to translate these insights into effective cancer therapies. The gene discussed is AARS1; the disease is cancer.