The dynamics of LDs reflect lipid metabolic status, and uncontrolled LD growth has been linked to the initiation of obesity LD biogenesis[28]; furthermore, nascent LDs are formed in the ER.[29, 30] Nascent LDs may become mature LDs by acquiring neutral lipids from the ER through their continuous association with this organelle.[31] RAB18 can promote LD growth by tethering the LDs to the ER through the interactions of SNARE and NRZ.[20] Analysis of the MS and Co‐IP data revealed that βFaar can bind to the GTPase RAB18, and βFaar overexpression significantly reduced the content of RAB18. Here, RAB18 is linked to obesity due to melanocortin 4 receptor deficiency.