BCL2L1(Bcl2 like 1)编码蛋白属于Bcl-2蛋白家族，Bcl-2蛋白家族成员通常形成异源或者同源二聚体，并作为抗凋亡或促凋亡调节因子参与多种细胞活动。该基因编码的蛋白位于线粒体外膜，并且显示可以调节线粒体外膜通道（VDAC）开口。 VDAC调节线粒体膜电位，从而控制活性氧的产生和线粒体释放细胞色素C，这两者都是细胞凋亡的有效诱导剂。选择性剪接导致编码两种不同的转录物变体。 较长的同种型BCL-XL充当凋亡抑制剂，较短的同种型BCL-XS充当凋亡激活剂。BCL2L1在结直肠癌（CRC）中常出现扩增，其表达水平影响不依赖于锚定的生长和细胞增殖，但目前没有足够证据说明它是肿瘤发生的驱动因素。

BCL2L1 (Bcl-2-like protein 1) belongs to the BCL-2 family of proteins and has a dual pro- and anti-apoptotic role ascribed to its different transcript isoforms produced by alternative splicing. The two isoforms, BCL-XL and BCL-XS, inhibit and activate apoptosis, respectively. BCL-XL sequesters activators of apoptosis such as BID, thus blocking downstream activation of the apoptosis effector proteins BAX and BAK, which normally control mitochondrial membrane potential and the release of cytochrome C. Inhibition of apoptosis by BCL-XL is overcome by caspase-mediated cleavage. Although the pro-apoptotic effect of BCL-XS is poorly understood, it has been shown to interact with BCL2 and BCL-XL. BCL2L1 is often amplified in colorectal cancers (CRC) and its expression affects anchorage-independent growth and cell proliferation, though it is not considered a driver of tumorigenesis. 

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