Myl6, also known as myosin light chain 6, is an essential light chain of myosin [3]. It plays significant roles in various biological processes. In platelets, it interacts with kindlin-3 and is required for integrin αIIbβ3 activation, which is crucial for hemostasis and thrombosis [3]. It may also be involved in pathways related to cell motility, as it has a functional connection with ADCK2 in melanoma cell motility [1].

In Myl6fl/flPF4-Cre mice with Myl6 deficiency in the megakaryocyte lineage, significant macrothrombocytopenia occurred due to defective proplatelet formation. Integrin αIIbβ3 activation and platelet aggregation were substantially impaired in these Myl6-deficient platelets [3]. Additionally, in non-alcoholic fatty liver disease (NAFLD), high-resolution analysis of mononuclear phagocytes highlighted the potential role of MYL6 in intrahepatic M1 phenotype Kupffer cells, and its elevated expression correlated with inflammation, oxidative stress, and disease severity [2]. In sepsis-induced acute lung injury, bioinformatics and experimental analyses confirmed increased mRNA levels of MYL6, and Mendelian randomization analysis revealed a causal relationship between MYL6 and sepsis [4].

In conclusion, Myl6 has diverse essential functions, especially in processes related to platelet function and in certain disease conditions such as NAFLD and sepsis-induced acute lung injury. Studies using Myl6-deficient mouse models have been instrumental in uncovering its role in these biological processes and disease areas.