A significant number of human tumors from diverse histological origins contain c-K-ras oncogenes which have been activated by somatic point mutations resulting in single amino acids substitutions in the encoded p21 ras protein. In addition to these qualitative changes, other genetic alterations leading to increased expression of the c-K-ras gene, especially its mutated form, appear to be important in the activation of its oncogenic potential. These findings support the hypothesis that c-K-ras oncogenes are contributing in a dominant but dose dependent manner to the multistage process of human tumorigenesis. Activated c-K-ras oncogenes have been detected in human tumors at different stages of progression, including premalignant neoplasms. These studies provide evidence for the involvement of somatic mutational activation of this ras gene in the early stages of tumor development in some types of human cancer. We discuss here the structural and functional features of the human c-K-ras gene and the involvement of its activated form in human cancer.