eceived her 1st renal transplant in 1989 for therapy of chronic glomerulonephritis. Her allograft failed in 1996 and renal function was replaced with intermittent hemodialysis until 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 ten mg/day since April 2015, when she seasoned myocardial infarction with implantation of stents in the coronary arteries. In April 2021, she was admitted to hospital due to SARS CoV-2 infection with consequent pneumonia, which was treated with remdesivir, ceftriaxone, and dexamethasone, also with tacrolimus reduction and mycophenolate cessation. A few days following discharge in the hospital, she created weakness of the proximal muscles from the arms and legs, which prevented her from finding up, walking, and leaning on her arms. In laboratory tests, there had been highly elevated levels of creatine kinase (CK) 9184 U/L (normal variety 153 U/L) and liver enzymes–alanine aminotransferase (ALT) 516 U/L (106) and aspartate aminotransferase (AST) 455 U/L (80). Hence, atorvastatin andF I G U R E 1 Modifications in CK, ALT, and AST values over 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 promptly excluded in the therapy, which resulted in comprehensive 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 didn’t uncover a pathological substrate that would clarify the muscular and liver lesion. Additional pharmacogenetic testing verified the reduced activity with the cytochrome P450 3A4 (CYP3A4) enzyme along with the patient getting an intermediate metabolizer of substrate MMP-3 list drugs–atorvastatin, tacrolimus, at the same time as remdesivir. Also, as outlined by the genotyping with the transport protein organic anion transporting polypeptides 1B1 (OATP1B1), there was a significant genetic predisposition for negative effects from the statin myotoxicity kind since the variant SCLO1B1 521CC final results in reduced statin transfer inside the liver. Depending on these findings, we concluded that myotoxicity and liver harm resulted from the mixture of therapy with tacrolimus, remdesivir, and higher doses of atorvastatin. The reported prices of critical adverse events among all statins as a class have been deficient accounting (1 ). Essentially the most common is actually a slight risk for the elevation of liver enzymes and myopathy [1]. The incidence of myopathy connected with statin therapy is dose-related. It is actually increased when statins are made use of in mixture with agents that share prevalent metabolic pathways such as other lipid-lowering agents (fibrates and niacin), as well as immunosuppressive drugs (cyclosporine A) [2]. Elevated systemic exposure to statins and consequent risk for complications has been reported in patients concomitantly treated with cyclosporin A with inhibition of drug PRMT5 Storage & Stability catabolism by cytochrome CYP3A4 or drug transport by P-glycoprotein (PGP) and organic anion transporting polypeptide OATP1B1 becoming related with this impact. It is actually not identified regardless of whether the combination of statins an