different transcription factors, FHL2 is itself involved extensively in regulating the expression of other genes. FHL2 exerts its transcriptional regulatory effects by functioning as an adaptor protein interacting indirectly with the targeted genes. In fact, LIM domain is a platform for the formation of multimeric protein complexes. Therefore, FHL2 can contribute to human carcinogenesis by interacting with transcription factors of cancer-related genes and modulates the signaling pathways underlying the expression of these genes. Different types of cancer are associated with FHL2 which act either as the cancer suppressor or inducer, for example in breast cancer, gastrointestinal (GI) cancers, liver cancer and prostate cancer. Clinical significance The expression and functions of FHL2 varies greatly depending on the cancer types. It appeared that phenomenon is highly related to the differential mechanistic transcriptional regulations of FHL2 in the various types of cancer. However, the participation of fhl2 mutations and the posttranslational modifications of fhl2 in carcinogenesis cannot be ignored. In fact, functional mutation of fhl2 has been identified in a patient with familial dilated cardiomyopathy (DCM) and is associated with its pathogenesis. This implied that fhl2 mutation may also profoundly affect the diverse cancer progressions. However, records describing the effects of fhl2 mutations on carcinogenesis are scarce. Phosphorylation of FHL-2 protein has no significant effects on FHL2 functioning both in vitro and in vivo. Provided that the existence of posttranscriptional modifications on FHL2 other than phosphorylation is still unclear and FHL2 functions almost exclusively through protein-protein interactions, research works in this direction is still interested. In particular, the mechanisms underpinning the subcellular localization of FHL2 should be focused. FHL2 can traffic freely between nuclear and the different cellular compartments. It also interacts with other proteinaceous binding partners belonging to different functional classes including, but not limited to, transcription factors and signal transducers. Therefore, FHL2 translocation could be important in regulating the different molecular signaling pathways which modify carcinogenesis, for example, nuclear translocation of FHL2 is related to aggressiveness and recurrence of prostate cancer Similar evidence also has been identified in experiment using A7FIL+ cells and NIH 3T3 cell line as the disease model. Breast cancer The FHL2 protein interacts with the breast cancer type 1 susceptibility gene (BRCA1) which enhances the transactivation of BRCA1. In addition, intratumoral FHL2 level was one of the factors determining the worse survival of breast cancer patients Gastrointestinal cancer FHL2 is related to gastrointestinal cancers and in particular,