We show that SLIT2/ROBO1 signaling can impact mTORC1 activity in two ways: (i) in a rapid, inducible manner, through addition of exogenous ligand, N-SLIT2, to macrophages which do not secrete SLIT proteins at a resting state (Dun et al, 2019; Wang et al, 2021), and (ii) in a constitutive manner, through basal auto/paracrine signaling in cervical cancer cells (HeLa) which express basal levels of SLIT2 and ROBO1 (Stella et al, 2009; Bianchi et al, 2021). Here, SLIT2 is linked to cervical carcinoma.