IGF1 and neoplasm: Treatment of HCC cells with the Insig1/2 loop 1 peptide disrupted the IGF1‐induced PCK1‐Insig1/2 interaction, PCK1‐mediated phosphorylation of Insig1 at S207 and Insig2 at S151, nuclear accumulation of SREBP1, SREBP1 activity, downstream lipid synthesis gene expression, lipid accumulation, and tumor cell proliferation.