A 60-year-old man started experiencing severe muscle pain, stiffness, and fatigue after being started on a statin.  Over eighteen months, he developed progressive, bilateral proximal lower limb and hand grip weakness and cramping.  He had a creatine kinase (CK) level of 18,674 U/L (normal <250) without pigmenturia, and elevated HMGCR antibodies (>200 Units, normal <20).  His statin was discontinued.  He was treated with methotrexate, rituximab, and high dose oral prednisone with partial response.  At presentation to our institution, neurological examination showed bilateral 4/5 grade muscle weakness and tenderness in iliopsoas, gluteus medius, pectoralis, and intrinsic hand muscles.  Needle electromyography showed rapid recruitment of short duration motor unit potentials, with fibrillation potentials, predominantly affecting axial and proximal muscles.  His CK value remained elevated at 1490 U/L; the HMGCR antibody titer decreased to 84 Units.  Quadriceps biopsy from his initial presentation demonstrated fiber size variability, few regenerating and necrotic fibers, tubular aggregates in type 2 muscle fibers and occasional cytoplasmic bodies.  CT scanning of his chest/abdomen/pelvis was negative for malignancy.  Next generation sequencing of 146 myopathy and 29 congenital myasthenic syndrome genes demonstrated no pathogenic or suspected pathogenic variants.  The patient was started on IVIG treatment to optimize response.