“…Lastly, as described above, the sites that the MICALs modify on actin (Met44 and/or Met47) have been linked to different diseases, including nemaline myopathy, CAP myopathy, aortic aneurisms, hypertrophic cardiomyopathy, intestinal hypoperistalsis, Baraitser-Winter cerebrofrontofacial syndrome, and ductus arteriosus (Laing et al, 2009;Hung et al, 2010b;Hoffjan et al, 2011;Zou et al, 2013;Regalado et al, 2014;Wangler et al, 2014;Yates et al, 2017;Zhang et al, 2019). It is also worth considering that some of the defects associated with mutations in the family of enzymes that reverse the MICAL's effects, MsrBs/SelR's, may result from increased effects of the MICALs on F-actin [see (Tarrago et al, 2022) for coverage of those defects].…”