AKT1 and cancer: Under insulin resistance, repression of FAM3C by the factors such as fatty acids will impair YY1‐HSF1‐Akt pathway to enhance hepatic gluconeogenesis and lipogenesis, exaggerating hyperglycaemia and fatty liver.27, 28 However, in case of TGFβ overproduction, long‐term activation of FAM3C‐YY1‐HSF1 pathway will trigger the development of cancers in various tissues including breast tissue by promoting excessive Akt activation.