While representing a commonly employed experimental process (119–122), it is highly likely that palmitate-induced insulin resistance is a complex multifactorial process that can involve multiple collateral signaling systems effects including altered ceramide levels (123), endoplasmic reticulum stress (124), mTOR/S6K activation (125), activation of protein phosphatase 2A (126), modulation of TNF-α signaling (127), and alterations in transmembrane free fatty acid receptor activity (128–130). The gene discussed is TNF; the disease is Insulin resistance.