## 1 Introduction  
Mantle cell lymphoma (MCL) is an aggressive subtype of non-Hodgkin B-cell lymphoma with an incidence of 5-7% among all lymphomas [1]. MCL is genetically characterized by the t(11;14) (q13;q32) translocation, which leads to constitutive overexpression of the _CCND1_ proto-oncogene due to the strong activity of the IgH enhancer juxtaposed near it, thereby leading to uncontrolled cell proliferation [2]. The majority of MCL cases are conventional MCLs (cMCLs) that are considered to originate from the neoplastic transformation of naive-like B-cells with no or a minimal number of _IGVH_ mutations, whereas cases of the leukemic non-nodal MCL (nnMCL) subtype originate from memory-like B-cells with the _IGVH_ gene mutated [3]. SOX11 transcription factor was reported to act as a proto-oncogene, which is overexpressed in all cMCLs corresponding to 90% of all MCLs [4]. MCL is an incurable malignancy despite recent advances in treatment options [5]. Standard therapeutic approaches such as immunocompetent/autologous stem cell transplantation may result in serious toxicity in MCL cases [6; 7]. More importantly, these traditional therapeutic approaches are still not effective against most relapsed MCL patients [8]. Despite the presence of clinical heterogeneity in MCL that requires more personalized approaches, these types of therapies do not take into account the genetic or transcriptional alterations in tumors of individual MCL patients. Novel therapies targeting aberrant signaling pathways (e.g., BCR signaling) or biological processes (e.g., apoptosis) are under development [9]. However, targeted treatment approaches for MCL patients are still not adequate to account for individual differences in the biomolecular characteristics of the individual patients. Consequently, there is an urgent need for the identification of novel oncogenes or tumor suppressor genes which promote the development and malignant progression of MCLs in different MCL patient subgroups. The prognosis of MCL may vary case-to-case; therefore, it is of utmost importance to identify patients bearing high risk in terms of prognosis and disease progression such that the most appropriate therapies can be applied with the correct timing. The MCL International Prognostic Index (MIPI), as well as the simplified MIPI risk score--which are based on the ECOG performance status, age, LDH levels, and white blood cell count--were established to identify high-, middle-, and low-risk group MCL patients [10]. The Ki67 proliferation index was reported to independently predict overall survival; hence, it is incorporated into MIPI, which is referred to as biological MIPI (MIPI-B) [11]. As these prognostic indices are not sufficient to account for the differences in the clinical outcome of MCL patients, researchers are seeking new prognostic biomarkers. As a part of this endeavor, a recent study proposed a circular RNA-based signature to predict good or inferior prognosis for MCL patients [12]. Several studies have previously revealed the genomic landscape of MCL tumors, which includes recurrent mutations in cancer-related genes such as _ATM_, _CCND1_, _TP53_, _NOTCH2_, or _RB1_[13; 14; 15; 16]. Mutations of _KMT2D_ and inactivation of _TP53_ through deletions or mutations have recently been reported to be associated with MCL progression and short overall survival [17]. Unlike genomic investigations, only a few transcriptomic studies have been performed with MCL cases. In one of these studies, recurrent _NOTCH1_ mutations were identified through analysis of whole transcriptome sequence data [18]. Another study proposed distinct molecular subsets of MCL identified through genomic and transcriptomic analyses [19]. Of significance, ILNK-A lncRNA was detected with qRT-PCR to be overexpressed in the plasma of MCL patients, and suggested as a candidate oncogene based on in vitro functional experiments [20]. Furthermore, it has recently been suggested to cause birutinib resistance in MCL cell lines [21].