Together with our previous work implicating the JNK/c‐Jun/BIM axis in obesity‐associated liver dysfunction,[37] our present data suggest that c‐Fos can dimerize with c‐Jun to modulate hepatic metabolism and insulin signaling.[37] Given the established roles of AP‐1 transcription factors in inflammation and transformation, it is plausible that c‐Fos–driven insulin resistance and lipotoxicity synergize with oncogenic pathways such as PI3K‐Akt and MAPK, facilitating the transition from steatosis to malignancy. The gene discussed is AKT1; the disease is obesity due to melanocortin 4 receptor deficiency.