Despite the presence of both ITIM and ITSM in PD-1, recruitment of SHP1 and SHP2 particularly to the ITSM motif of PD-1 is instrumental in mediating inhibitory functions of PD-1.1, 2 Furthermore, the fact that PD-1 is capable of suppression of PI3K/AKT activation was mainly due to its ITSM added further importance to this domain in mediating PD-1 signal transduction.2 Indeed our co-immunoprecipitation studies supported the notion in providing evidence of stronger association of SHP2 with PD-1, which was markedly inhibited during infection. Here, PTPN11 is linked to infection.