Indeed, it has been observed that CRC cells derived from primary tumors or metastases undergo differential modulation of metabolic capacities in the presence of acute oxidative H2O2 distress or eustress, such that they can utilize canonical and non-canonical Wnt/β-catenin/APC molecular pathways also in crosstalk with the c-Jun N-terminal kinase (JNK) pathway [34,35]. This evidence concerns the gene APC and colorectal carcinoma.