C1qb, also known as Complement C1q Subunit B, is a crucial component of the complement system. The complement system is an essential part of the innate immune response, playing a significant role in processes such as inflammation, immune complex clearance, and cell lysis. C1q, composed of C1QA, C1QB, and C1QC, initiates the classical complement pathway [8].

In various disease contexts, C1qb has been implicated. In primary refractory diffuse large B cell lymphoma, cholesterol efflux from C1QB-expressing macrophages was associated with resistance to chimeric antigen receptor T cell therapy, as it inhibited CAR-T cells' cytotoxicity by inducing an immunosuppressive state in CD8+ T cells [1]. In colorectal cancer, forward Mendelian randomization analysis indicated that C1QB was a risk factor for CRC, suggesting its oncogenic role [2]. In skin cutaneous melanoma, high levels of C1QB expression were associated with favorable prognosis, and C1QB was identified as one of the core tumor microenvironment-related genes [3,8]. In type 1 diabetes mellitus, silencing C1QB inhibited the differentiation of monocytes into macrophages, reduced the number of macrophages, and alleviated pancreatic islet β-cell damage [4]. In diabetic nephropathy, C1QB was identified as a potential candidate gene for diagnosis [5]. In intrahepatic cholangiocarcinoma, an APOE + C1QB+ macrophage subtype was associated with a poor prognosis [6]. In psoriasis complicated with atherosclerosis, C1QB was identified as an important hub gene [7].

In conclusion, C1qb is integral to the complement system and has diverse functions in multiple disease conditions. Research on C1qb, especially through genetic models like gene knockout, could potentially provide deeper insights into the disease mechanisms and offer new therapeutic strategies for diseases such as lymphoma, colorectal cancer, melanoma, diabetes, and related complications.