FHIT and neoplasm: The unrepaired and aberrantly repaired DNA lesions that result from DNA damage can thus accumulate in the oncogene expressing tumour cells, leading to genomic instability and malignant progression.’ The results of the experiments described here suggest the conclusion that loss of Fhit protein function results in acquisition of features similar to those of an oncogene-transformed cell: protection from apoptosis, rapid activation of DNA damage checkpoint and accumulation of mutations due to lesion misrepair.