In thyroid cells, it was reported (Cass et al, 1999) that activation of PI3K confers a TSH independent DNA synthesis, and it was demonstrated (Gire et al., 2000) that in primary human thyroid cells PIK3 is an absolute requirement for the proliferative response to RAS. RAS-activating point mutations are reported to occur at a high frequency (from 55 to 100%) in undifferentiated thyroid cancers (Suárez, 1998), and thus it is conceivable that an increase in PI3K copy number is implicated in proliferative advantage in these tumours. The gene discussed is PIK3CG; the disease is thyroid cancer.