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. Here, PIK3CG is linked to neoplasm.