[18], who found that ASD infants at 9-12 months showed reduced alternating gaze to initiate JA, but they did not show a reduced orienting to social faces (social gaze). The authors concluded that social motivation is not a primary deficit in ASD [18; 19]. In contrast to the \"Social Motivation Model\", other authors argued that JA alterations in ASD may be linked to atypicalities in the executive attention system that underlies the orienting response, which implies the ability to disengage the attention from a central stimulus and to subsequently orient it to a new target [19; 20; 21]. During a typical JA episode, one has to rapidly shift the attentional focus from an object or an event to the social partner's face and back again toward the object or event he/she wants to share with the social partner. While JA skills begin to emerge from 6 months of life, with a high rate of variability among individuals [10], the ability to flexibly switch visual attention matures rapidly during the first months of life and allows infants to quickly and selectively orient towards salient stimuli and thus to learn from the environment [22]. Atypical reorienting efficiency during the first year of life has been associated with the later emergence of ASD [8; 23]. Reorienting visual attention can be conceptualized as the time taken by the infant to make a saccade from a central stimulus to a peripheral one. Saccadic movements are driven by the visual attention system that selects the direction of each saccade by disengaging attention from a fixation point and shifting it to another point. The neural mechanisms underlying impaired attentional disengagement in ASD remain poorly understood. However, elevated levels of tonic locus coeruleus-norepinephrine activity may play a role [24], as well as atypical activation and connectivity of the ventral and dorsal subdivision of the anterior insula, which is supposed to regulate the salience network involved in the regulation of attention [25]. In summary, a reduction in the efficiency of the attention disengagement and in the frequency of joint attention during the first year of life can be considered as supporting evidence for both of the explanatory theories described above. Recent research has focused on attentional processes in ASD using eye-tracking (ET) a non-invasive methodology designed to provide an objective quantification of eye movements [26; 27; 28; 29; 30]. The precision and cost effectiveness of ET render it a promising tool for the identification of biomarkers useful for clinical trials [31] and the examination of processes associated with autism symptoms [32; 33]. A substantial body of scientific literature hasdemonstrated that eye tracking can be considered a valid and reliable methodology, especially in very young subjects or those with severe clinical impairments who exhibit lower levels of cooperation [28; 33; 34; 35]. Several studies analyzed the reorienting efficiency, more specifically the disengagement of attention, through ET in infants at risk for ASD and documented that attentional patterns differ between infants subsequently diagnosed with ASD and neurotypical peers, with the former displaying increased saccadic latencies as early as 7 months of life [36] and continuing to show this pattern during the second year of life [37]. Additional studies have generated mixed findings, perhaps reflecting variability in methodological paradigms and tasks, including whether the stimuli used to measure disengagement latencies are social or non-social in nature. Accordingly, the nature and the complexity of the stimuli (e.g., faces and objects) could affect the disengagement of attention, making it difficult to ascertain whether altered disengagement reflects altered social processing (i.e., longer latency specifically in response to social stimuli such as faces) versus a basic impairment of attentional disengagement (regardless of the nature of the stimuli being attended to) [38].