eceived her first renal transplant in 1989 for remedy of chronic glomerulonephritis. Her allograft failed in 1996 and renal function was replaced with intermittent hemodialysis till the second transplantation, which was performed in January 2001. She was treated with triple immunosuppressive therapy–tacrolimus, mycophenolate mofetil, and steroids. Also, in chronic therapy, she had atorvastatin 80 mg/day and ezetimibe 10 mg/day considering the fact that April 2015, when she knowledgeable myocardial infarction with implantation of stents inside the coronary arteries. In April 2021, she was admitted to hospital as a result of SARS CoV-2 infection with consequent pneumonia, which was treated with remdesivir, ceftriaxone, and dexamethasone, also with tacrolimus reduction and mycophenolate cessation. Several days just after discharge from the hospital, she developed weakness of your proximal muscles of your arms and legs, which prevented her from obtaining up, walking, and leaning on her arms. In laboratory tests, there have been highly elevated levels of creatine kinase (CK) 9184 U/L (typical variety 153 U/L) and liver enzymes–alanine aminotransferase (ALT) 516 U/L (106) and aspartate aminotransferase (AST) 455 U/L (80). Thus, atorvastatin andF I G U R E 1 Changes in CK, ALT, and AST values more than time, relative to drug administration and exclusion (remdesivir, atorvastatin, ezetimibe, and tacrolimus)2021 International Society for Apheresis, Japanese Society for Apheresis, and Japanese Society for Dialysis Therapy 478 wileyonlinelibrary/journal/tap Ther Apher Dial. 2022;26:47879.LETTER To the EDITORezetimibe have been immediately excluded from the therapy, which resulted in complete normalization levels of CK and liver enzymes (ALT and AST) and regression of symptoms (Figure 1). The performed immunological, virological, hepatological, and neurological diagnostic tests did not come across a pathological substrate that would explain the muscular and liver lesion. Further pharmacogenetic PLK4 list testing verified the reduced activity in the cytochrome P450 3A4 (CYP3A4) enzyme plus the patient getting an intermediate metabolizer of substrate drugs–atorvastatin, tacrolimus, also as remdesivir. Also, based on the genotyping of your transport protein organic anion transporting polypeptides 1B1 (OATP1B1), there was a significant genetic predisposition for unwanted side effects on the statin myotoxicity kind because the variant SCLO1B1 521CC benefits in lowered statin transfer inside the liver. Determined by these findings, we concluded that myotoxicity and liver harm resulted in the PKCθ site mixture of therapy with tacrolimus, remdesivir, and high doses of atorvastatin. The reported prices of critical adverse events among all statins as a class have already been deficient accounting (1 ). By far the most prevalent is really a slight threat for the elevation of liver enzymes and myopathy [1]. The incidence of myopathy related with statin therapy is dose-related. It really is increased when statins are applied in combination with agents that share common metabolic pathways which include other lipid-lowering agents (fibrates and niacin), as well as immunosuppressive drugs (cyclosporine A) [2]. Elevated systemic exposure to statins and consequent threat for complications has been reported in sufferers concomitantly treated with cyclosporin A with inhibition of drug catabolism by cytochrome CYP3A4 or drug transport by P-glycoprotein (PGP) and organic anion transporting polypeptide OATP1B1 getting connected with this effect. It really is not recognized whether or not the mixture of statins an