WHAMM is a nucleation-promoting factor that stimulates Arp2/3 complex-mediated actin polymerization at the Golgi apparatus and along tubular membranes 1. It coordinates actin-nucleating and microtubule-binding activities to drive membrane tubule elongation and regulate Golgi positioning 2. WHAMM participates in vesicle transport between the endoplasmic reticulum and Golgi complex and is required for RhoD-dependent actin reorganization in cell adhesion and migration. At the cellular level, WHAMM controls autophagosome membrane closure and cargo sequestration through Arp2/3 complex-mediated actin assembly 3. It also regulates cell death by controlling actin-mediated cytochrome c release from mitochondria and ASC speck formation 4. WHAMM forms a complex with RHOD to facilitate ATG9A trafficking and autophagosome formation during starvation 5. Additionally, WHAMM and JMY are necessary for rapid DNA damage-induced apoptosis through a p53-dependent pathway 6. Clinically, WHAMM is identified as a key kidney disease risk gene; variants on chromosome 15 regulate WHAMM expression, which is elevated in chr15 and acute kidney disease 4. WHAMM knockout mice display kidney proximal tubule abnormalities and impaired nutrient reabsorption, with elevated urinary albumin, glucose, phosphate, and amino acids 3. These findings reveal WHAMM's essential role in maintaining kidney function and controlling cellular proteostasis.