Immune/inflammatory cells infiltrate almost all human solid tumors and affect all stages of carcinogenesis as they produce different cytokine subsets. The overproduction of T(H)17 cytokines marks the early stages of colorectal carcinoma (CRC) and negatively influences the prognosis of CRC patients. Studies with murine models of CRC have delineated the mechanisms by which T(H)17 cytokines, notably, interleukin (IL)-17A, IL-17F, IL-21, and IL-22, regulate oncogenesis and tumor progression, paving the way to the development of novel anticancer drugs. In this review article, we discuss experimental data supporting the role of T(H)17 cytokines in the modulation of colorectal tumorigenesis.