Over‐expression of IGF‐II mRNA in tumors has been attributed to loss of imprinting and mutations in tumor suppressor genes, possibly including loss of heterozygosity (LOH) at the M6P/IGF‐IIR locus.5, 55 In IGF‐II over‐expressing tumors the subsequent processing of the pro‐peptide may be disturbed, leading to the accumulation of high MW forms of IGF‐II, part of which is secreted into the circulation. Here, IGF2 is linked to neoplasm.