We have previously reported that carboxyl terminal truncations of the normal human fyn gene, a member of the src subfamily, can transform immortal mouse fibroblasts to full malignancy. In search of evidence which suggests the possible activation of the human fyn gene, we have screened DNAs and RNAs from a number of human tumor cell lines. The results indicate that the fyn gene is not frequently changed grossly in the naturally occurring tumors. To establish a basis for understanding the physiological function(s) of this highly conserved gene, we have prepared specific antibodies to the fyn-encoded proteins. Using them we have shown the presence of fyn proteins in human lymphocytes and monocytes and their protein-tyrosine kinase activity.