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complexes known as mTORC1 and mTORC2 [5]. mTORC1 is the major regulator of survival, growth, proliferation and motility, in response to mitogens, energy and nutrient levels [6]. Due to its central role in cellular functions, mTORC1 dysregulation is involved in a number of inflammatory or neoplastic conditions [7]. Upregulation of mTORC1 has also been observed in common inflammatory dermatoses, such as psoriasis, acne vulgaris and HS [8–10]. The mTORC1 pathway is of pivotal importance for metabolic regulation and functioning of innate and adaptive immune cells as clearly verified by the immune-suppressive function of mTORC1 inhibitors such as rapamycin [11]. In particular, mTORC1 signalling has been found to play a crucial role in the control of macrophage metabolism and activation [12]. In fact, macrophage activation is associated with metabolic shifts and metabolic reprogramming that enable bioenergetic and biosynthetic support as well as regulatory control of macrophage activities [13, 14]. In response to different stimuli, macrophages can differentiate into either a pro-inflammatory subtype (M1, classically activated macrophages) or acquire an anti-inflammatory phenotype (M2, alternatively activated macrophages). The metabolism of M1 macrophages is characterized by enhanced glycolysis, flux through the pentose phosphate pathway (PPP), fatty acid synthesis, and a truncated tricarboxylic acid cycle, leading to accumulation of succinate and citrate. The metabolic profile of M2 macrophages is defined by oxidative phosphorylation, fatty acid oxidation, a decreased glycolysis, and PPP [15]. Interestingly, the mTOR signalling enhances aerobic glycolysis [16]. In addition, mTORC1 promotes the synthesis of lipids and proteins in growing and proliferating cells. Lipid synthesis requires citrate production as well as activation of Srebp1, the transcriptional regulator of lipogenesis. Srebp1 is activated by mTORC1 in macrophages. Expansion of the ER and Golgi compartments, which has been linked I have read with interest the paper by Shah and colleagues [1]. The authors have underlined that macrophages play a critical role in the pathogenesis of hidradenitis suppurativa (HS). Dysregulation of macrophage activity is a big culprit in causing chronic tissue inflammation and damage. More specifically, dysregulated activation and proliferation of macrophages contribute to elevated macrophage secretion of pro-inflammatory cytokines and matrix metalloproteases (MMPs), which activate other inflammatory effectors and directly lead to tissue injury. In particular, macrophages are the most numerous inflammatory cells found in HS infiltrate and release numerous pro-inflammatory cytokines such as interleukin (IL)-23 [2], IL-1b [3] and tumour necrosis factor (TNF)-alpha [3, 4], which work to further enhance the inflammation. As a result, macrophages may modify the pericellular environment by influencing other inflammatory cells and may act as key players in the pathogenesis of the disease. This evidence helps to understand why HS patients often have concurrent inflammatory conditions which are also characterized by macrophage dysfunction such as Crohn’s disease and spondyloarthropathy. The authors have also tried to identify molecular players and lifestyle factors which may contribute to macrophage dysregulation in HS. In this regard, I think that altered mechanistic target of rapamycin complex 1 (mTORC1) signalling may contribute to macrophage dysregulation in HS. mTOR belongs to the phosphatidylinositol 3-kinase-related kinase protein family and forms at least two multiprotein Inflammation Research