In the tumor microenvironment (TME), lactate accumulation and its subsequent lactylation of IGF2BP3 were discovered to upregulate the expression of PCK2 and NRF2, thereby instigating serine metabolic reprogramming, augmenting the availability of S-adenosylmethionine (SAM), and conferring drug resistance in hepatocellular carcinoma (31). Here, IGF2BP3 is linked to neoplasm.