In the present work, we demonstrated that the pharmacological inhibition of p32/C1QBP, using the small molecular inhibitor M36, induced, in a dose-dependent manner, a significant decrease in the viability, proliferation rate, and clonogenic capacity of different colon cancer cell lines overexpressing C1QBP, consistent with our previous studies highlighting p32/C1QBP as an important oncogene that promotes a malignant phenotype in colon cancer cells [28]. This evidence concerns the gene C1QBP and colonic neoplasm.