manner and protected the spinal cord against motor neuron death. stx2-producing e. coli-associated encephalopathy model shiga toxin-producing escherichia coli (stec) causes hemorrhagic colitis, hemolytic uremic syndrome, and acute encephalopathies that may lead to sudden death or severe neurologic sequelae. severely immunocompromised non-obese diabetic/severe combined immunodeficiency (nod-scid) mice orally inoculated with 9 × 10^9 colony-forming units of stec o111 and treated 48 h later with intravenous injection of 5 × 10^4 muse cells exhibited 100% survival and no severe after-effects of infection. suppression of granulocyte-colony-stimulating factor (g-csf) by rnai abolished the beneficial effects of muse cells, leading to a 40% death and significant body weight loss, suggesting the involvement of g-csf in the beneficial effects of muse cells in stec-infected mice. thus, intravenous administration of muse cells could be a candidate therapeutic approach for preventing fatal encephalopathy after stec infection. corneal scarring human muse cells, collected from lipoaspirate, were activated by forming spheroid in the dynamic rotary cell culture system. these activated muse spheroids enabled ready differentiation into corneal stromal cells (cscs) expressing characteristic marker genes and proteins in vitro. implantation of muse cells–differentiated cscs (muse-cscs) laden assembled with two orthogonally stacked stretched compressed collagen (cell-scc) in mouse and tree shrew wounded corneas prevented the formation of corneal scarring, increased corneal re-epithelialization and nerve regrowth, and reduced the severity of corneal inflammation and neovascularization. cell-scc retained the capacity to suppress corneal scarring after long-distance cryopreserved transport. muse cells in clinical data muse cells are present in the human bone marrow of healthy donors. the number of peripheral blood-muse cells is drastically elevated in stroke patients 24 h after onset. in acute myocardial infarction patients, peripheral blood-muse cells significantly increase 24 h after onset, concomitant with an increase in serum sphingosine-1-phosphate, and return to baseline levels with 2~3 weeks. importantly, patients with an increased peripheral blood-muse cell number in the acute phase show cardiac function recovery and avoidance of heart failure at 6 months after onset, suggesting the reparative function of endogenous muse cells. regenerative medicine bone marrow transplantation: muse cells are a subpopulation of bone marrow cells. they represent a small population of mono-nucleated bone marrow cells (~0.03%). this means that they have already been supplied to patients many times all over the world in bone marrow transplantations; a well-known procedure that has been performed in clinics since 1958. mesenchymal stem cell transplantation: muse cells exist within cultured mscs such as bone marrow mesenchymal stem cells and adipose-derived stem cells. msc transplantation has been employed for repairing liver, heart, neural tissue, airway, skin, skeletal muscle, and intestine. therefore, if muse cells were purified or enriched, the effectiveness of currently performed msc transplantation is expected to see vast improvements. because muse cells do not form teratomas in vivo, they could provide an ideal source of pluripotent stem cells for regenerative medicine and cell-based therapy. clinical trial currently, life science institute, inc. and its parent company, mitsubishi chemical holdings, have established a cell-processing procedure that is compliant with the japanese good manufacturing practice (gmp) and good gene, cellular, and tissue-based products manufacturing practice (gctp) regulation. clinical trials for human muse cell-based product cl2020 have been started in 2018, targeting acute myocardial infarction, stroke, epidermolysis bullosa, spinal cord injury, amyotrophic lateral sclerosis and acute respiratory distress syndrome (ards) related to novel coronavirus (sars-cov-2) infection. rapid communications for acute myocardial infarction and epidermolysis bullosa have been published. the summary results of a randomized double-blind placebo-controlled clinical trial in patients with stroke was announced. the primary endpoint of the clinical trial was patient safety for up to 52 weeks after administration of cl2020 and no adverse events that would prevent advancement of the clinical study were observed throughout the clinical study period. prior to administration of placebo or cl2020, most patients had a modified rankin scale (mrs1)) score of 4 (moderately severe disability: unable to walk and attend to bodily functions without assistance) or 5 (severe disability:bedridden, incontinent, and requires continuous care and attention). at 52 weeks after administration, the proportion of responders in the cl2020 group was 68.2% (15/22 cases), and the difference between the cl2020 group and the placebo group (37.5%, 3/8 cases) was maintained at more than 30%.evaluation of the efficacy at 52 weeks after administration revealed that 7 of 22 (31.8%) subjects in the cl2020 group achieved an mrs score of 1 (no significant disability despite symptoms: able to carry out all pre-stroke activities without assistance, such as return to work). no one in the placebo group achieved an mrs score of 1 within 52 weeks.