## 1 Introduction  
Shift work (SW) comprises a work schedule that involves recurring times of nonstandard work hours balanced to a fixed daily work plan with regular day work times [1, 2]. SW can include early morning, afternoon, evening, or night shifts and may be scheduled to fixed or rotational (i.e., rotating among mornings, afternoons, and nights) timetables [2]. In Europe, it has been estimated that 17% of workers [3] are implicated in SW, and the number is always increasing, due to new job demands [4]. In 2007, the International Agency for Research on Cancer (IARC) classified shift work (SW) as \"probably carcinogenic to humans\" (Group 2A) and more recently, in 2019, IARC classified Night Shift Work (NSW) as \"probably carcinogenic to humans\" (Group 2A) by [5] for breast, prostate, and colon, founded on limited evidence of cancer in humans, sufficient evidence of cancer in experimental animals, and strong mechanistic evidence in experimental animals [5]. SW, mainly the category linking working at night, is correlated with circadian rhythm disruption that determines trouble falling asleep, shortened sleep, and daytime fatigue [2, 6, 7]. Moreover, several investigations have highlighted that SW [8, 9] and misalignment of sleep [10] may affect cognitive functions. SW may modify lifestyle features, which could be a factor in the pathway between SW and cognitive performances [1, 11]. Recently, it was demonstrated that SW might have effects on biological aging [12]. Recently, many researchers have focused their attention on the genes of the circadian clock, a sequence of genes implicated on preserving the inside organization of numerous oscillators inside and among organs systems [13]. The Circadian Locomotor Output Cycles Kaput (_CLOCK_) gene is wildly investigated for this purpose: it codifies for the _CLOCK_ protein, a favorable regulatory hand of the circadian system [13]. Variations of the _CLOCK_ gene are usually given by SW and sleep deprivation or by the genetic distinction of the _CLOCK_ gene [14]. This modification has been correlated with numerous physiological and pathological issues [14]. Notably, disparities of the _CLOCK_ gene have been correlated with the initiation of obesity, type 2 diabetes, sleep and mood diseases, and cancer [15; 16; 17]. Concerning aging, a low number of investigations have studied the potential role of the _CLOCK_ gene on longevity or aging [18; 19]. Aging is a physiological progression that causes significant alterations in biological variables and organ functions. Some investigations have underlined a function of the _CLOCK_ gene on several features of the life span development, recommending a probable link among this gene and aging [20; 21; 22]. The protein encodes a transcription agent of the basic helix-loop-helix (bHLH) family and includes DNA required for the activity of histone acetyltransferase. The ARNTL (BMAL1), an encoded protein structure, attaches E-box enhancer elements upstream of Period (PER1, PER2, PER3) and Cryptochrome (CRY1, CRY2) genes, and starts transcription of those genes. PER and CRY proteins heterodimerize and downstream theirs possess transcription by cooperating in a feedback loop with _CLOCK_/ARNTL complexes [20; 21; 22; 23]. Some researchers support that SW may affect in aging acceleration, as it has been correlated with a higher risk of longevity diseases [22]. History of SW was correlated with age acceleration in epigenetic _CLOCK_[23; 24]. More recently, [PERSON] et al. [25] suggest that SW may initiate a range of modifications in DNA methylation, as well as modifications at specific CpG sites and epigenetic age [25] and the latter is associated with age acceleration [23; 24; 25; 26; 27; 28]. Over the years, it has been tried to find biomarkers to evaluate biological aging, such as oxidative damage, mitochondrial oxygen dissipation, neuroendocrine secretion levels, cyclin-dependent kinase inhibitor expression, and telomere length [23; 27; 29; 30; 31].