Tm9sf1, also known as MP70 and HMP70, is a member of the nine-transmembrane superfamily proteins. It has been implicated in various biological functions such as autophagy regulation, which is an important cellular process involved in degradation of proteins and organelles, and is associated with multiple diseases [2,3,4,5,6].

In disease-related research, Tm9sf1 knockout mouse models have provided valuable insights. In rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) models, Tm9sf1-/-mice produced fewer autoantibodies and showed reduced disease severity. TM9SF1 levels in patients' peripheral blood mononuclear cells were positively linked with autoantibody titers and pro-inflammatory cytokine levels, and could predict disease activity [1]. In acute lung injury (ALI) mouse models, Tm9sf1 knockout significantly alleviated LPS-induced ALI, with higher survival rate, improved pulmonary vascular permeability, decreased inflammatory cell infiltration, and downregulated inflammatory cytokines. TM9SF1 was a negative regulator of autophagy in this model [3]. In colorectal cancer models, Tm9sf1 knockout increased tumor numbers and size and enhanced tumor invasion, while TM9SF1 suppressed metastasis by targeting Vimentin for autophagic degradation [4].

In conclusion, Tm9sf1 plays essential roles in autophagy-related biological processes. The study of Tm9sf1 knockout mouse models has revealed its significance in autoimmune diseases like RA and SLE, as well as in inflammatory conditions such as ALI and in cancer metastasis. These findings provide potential therapeutic targets for the treatment of related diseases.