## 1 Introduction  
Breast cancer is a result of random mutations that allow breast cells to grow and proliferate without the tight restrictions imposed on them during the cell cycle [1]. These mutations affect several of the cells' homeostatic parameters, including their cellular metabolism, proliferation rate, and the defenses they establish to circumvent cell cycle arrest or controlled death [1]. Given this, breast cancers can be categorized into four groups based on genetic information: luminal \(A\), luminal B, HER2-positive, and triple-negative. These four types, as seen in Table 1, are classified based on whether or not the cancer cells possess (1)the human epidermal growth factor receptor 2 (HER2) protein, a type of transmembrane receptor tyrosine kinase and (2) hormone receptors, including estrogen receptors (ER) and/or progesterone receptors (PR), within the cell membrane [1]. Luminal A breast cancers, such as the MCF-7 cell line, are HER2-negative and hormone receptor-positive [2]. These cancers tend to grow slowly due to low levels of Ki-67, a tumor proliferative marker that helps control the pace of the cell growth by preventing the aggregation of mitotic chromosomes [2; 3]. Luminal B breast cancers, such as the BT-474 cell line, are hormone receptor-positive, and either HER2-negative or -positive, with high levels of Ki-67 [2]. HER2-positive breast cancer, as the name suggests, is HER2-positive and hormone receptor-negative [4]. SK-BR-3 falls under HER-2 classification. Triple-negative breast cancers, such as MDA-MB-231, do not express any of the three main receptors, making it more aggressive and difficult to treat than the other breast cancers [5]. Receptor status determines the initial prognosis and the ensuing treatment of the cancer since certain subtypes do not respond to targeted hormone therapies. Many standard systemic and localized cancer treatments are unable to precisely kill microscopic disease around the tumor site and often affect healthy adjacent tissue [6; 7]. In the case of chemotherapy and endocrine therapy, these treatments also worsen the quality of life to a greater extent and for a longer period of time [8]. However, some modern treatments not only work to actively kill cancer cells but also mitigate the chance of recurrence after tumor resection without worsening the patient's quality of life [9; 10]. One such treatment is through the use of cold atmospheric plasma (CAP). CAP is a room temperature ionized gas, generating a composite of charged particles, photons, and an electric field [11]. CAP also gives rise to a cellular environment rich in reactive oxygen species (ROS) and reactive nitrogen species (RNS). Major CAP-generated ROS include ozone (O\({}_{3}\)), singlet oxygen (\({}^{1}\)O\({}_{2}\)), superoxide anion (O\({}_{2}\)'-), and hydroxyl radical (OH). The major RNS generated include nitric oxide ('NO) and nitric dioxide (NO\({}_{2}\)) [12]. These reactive species yield peroxynitrite (ONOO-), hydroxide (H\({}_{2}\)O\({}_{2}\)), and nitrite (NO\({}_{2}\)\({}^{-}\)) when in contact with bodily fluid or a cell culture medium [13]. Excess cellular levels of these species can lead to the activation of apoptosis due to the damage they cause to mRNA [14], vital proteins, nucleic acids, lipids, membranes, and organelles [15]. During apoptosis signaling, caspase precursors undergo rapid proteolytic processing and activation [16]. Activated caspases function to hydrolyze key enzymes and degrade cellular proteins necessary for the survival and growth of the cell, resulting in cell death [16]. Additionally, a decrease in mitotic cell division and a reduction of Ki-67 expression in tumor cells could indicate CAP-induced cell death post treatment. Ki-67 is a nuclear protein that is expressed in actively proliferating cells during all phases of the cell cycle [17]. CAP prompts a decrease in Ki-67 as it is known to selectively induce apoptosis and cell cycle interruption [18].