TBC1D4 and Insulin resistance: Our second hypothesis regarding the mechanism of muscle insulin resistance linked to acute inactivity is the decreased phosphorylation of Rab‐GTPase‐activating protein (GAP), that is, AS160 (Akt substrate of 160 kDa; also known as TBC1D4) and its paralog TBC1D1 (tre‐2/USP6, BUB2, cdc 16 domain family member 1).