In recent years, emerging evidence highlights the roles of Wnt in regulating and reprogramming tumor cell metabolism.[37] The linear correlation of PC and β‐catenin expression (CTNNB1) in the TCGA co‐expression database suggests the crosstalk of PC and Wnt signaling in multiple cancer types (Figure S6A, Supporting Information).[38] Given the effects of the Wnt pathway on cancer metabolism, we hypothesized that PC and known upstream Wnt/β‐catenin/Snail signaling could be mutually modulated in anaplerosis. This evidence concerns the gene SNAI1 and neoplasm.