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CAMK2B‐mediated phosphorylation of FAM134B (1) enhances its self‐association and oligomerization (2), thus promoting ER membrane fragmentation (3) and the ER‐phagy process (4). FAM134B oligomerization can be pathologically enhanced in type II HSAN syndrome due to G216R mutation in the RHD of FAM134B. As a consequence, an excessive ER fragmentation and ER‐phagy may promote neuronal cell death through unknown mechanisms.
